bims-cagime Biomed News
on Cancer, aging and metabolism
Issue of 2025–10–19
43 papers selected by
Kıvanç Görgülü, Technical University of Munich



  1. Clin Cancer Res. 2025 Oct 14.
       PURPOSE: Treatment of pancreatic ductal adenocarcinoma (PDAC) has been advanced by the development of KRAS inhibitors. Despite this progress, PDACs invariably develop resistance to these agents by multiple different mechanisms. Here, we investigated the role of the oncogenic MUC1-C (M1C) protein in mediating resistance of PDAC cells to KRAS inhibition.
    EXPERIMENTAL DESIGN: Three PDAC KRAS G12D mutant cell lines, as well as patient-derived KRAS inhibitor resistant organoids and PDX models were investigated in these studies. An anti-M1C antibody-drug conjugate (M1C ADC) was evaluated for in vitro and in vivo activity. PDAC patient tumors were studied by single cell RNA sequencing and immunohistochemical (IHC) staining.
    RESULTS: The MUC1 gene is upregulated in PDAC KRAS G12D-mutant tumors. We report that treatment of PDAC cells with the KRAS G12D inhibitor MRTX1133 is associated with induction of the M1C protein. Mechanistically, KRAS G12D inhibition induces M1C by activation of an M1C/NF-kB p65 auto-inductive pathway. Our results further demonstrate that M1C drives resistance to MRTX1133 by activating the inflammatory IFN type I pathway. Targeting M1C genetically and pharmacologically thereby reverses MRTX1133 resistance and is synergistic in combination with MRTX1133 treatment. Of translational significance, we demonstrate that a M1C ADC is highly effective against MRTX1133-resistant PDAC KRAS G12D cell lines and patient-derived organoid and PDX models.
    CONCLUSIONS: These findings demonstrate that M1C confers resistance of PDAC to KRAS G12D inhibition and identify M1C as a potential target for ADC treatment of PDAC patients who are refractory to KRAS inhibitors.
    DOI:  https://doi.org/10.1158/1078-0432.CCR-25-2333
  2. Mol Cell Proteomics. 2025 Oct 13. pii: S1535-9476(25)00188-4. [Epub ahead of print] 101089
      Protein glycosylation plays a pivotal role in various biological processes, and the analysis of intact glycopeptides (IGPs) has emerged as a powerful approach for characterizing alterations in protein glycosylation associated with diseases. Despite the critical insights gained from IGP analysis, dedicated databases, and specialized tools for comprehensive glycoproteomics remain scarce. In response to this deficiency, we developed "Glycoprotein-Notebook", an online resource that consolidates the mass-spectrometry evidence for intact glycopeptides identified from 10 cancer types studied in the Clinical Proteomic Tumor Analysis Consortium (CPTAC) projects and provides analytical tools for in-depth glycopeptide characterization. Using Pancreatic Ductal Adenocarcinoma (PDAC) as a case study, we validated and showcased the toolkit's analytical capabilities. Our results underscore the promise of IGPs as cancer-specific diagnostic and therapeutic targets. Accordingly, Glycoprotein-Notebook emerges as a valuable resource for cancer researchers exploring the intricate relationship between protein glycosylation and cancer phenotypes.
    Keywords:  Cancer; Database; Glycopeptides; Glycoproteomics; Mass spectrometry; Pancreatic Ductal Adenocarcinoma (PDAC)
    DOI:  https://doi.org/10.1016/j.mcpro.2025.101089
  3. Cell Metab. 2025 Oct 10. pii: S1550-4131(25)00434-6. [Epub ahead of print]
      Solute carriers (SLCs) regulate cellular and organismal metabolism by transporting small molecules and ions across membranes, yet the physiological substrates of ∼20% remain elusive. To address this, we developed a machine-learning platform to predict gene-metabolite associations. This approach identifies UNC93A and SLC45A4 as candidate plasma membrane transporters for acetylglucosamine and polyamines, respectively. Additionally, we uncover SLC25A45 as a mitochondrial transporter linked to serum levels of methylated basic amino acids, products of protein catabolism. Mechanistically, SLC25A45 is necessary for the mitochondrial import of methylated basic amino acids, including ADMA and TML, the latter serving as a precursor for carnitine synthesis. In line with this observation, SLC25A45 loss impairs carnitine synthesis and blunts upregulation of carnitine-containing metabolites under fasted conditions. By facilitating mitochondrial TML import, SLC25A45 connects protein catabolism to carnitine production, sustaining β-oxidation during fasting. Altogether, our study identifies putative substrates for three SLCs and provides a resource for transporter deorphanization.
    Keywords:  SLC25A45; SLC45A4; UNC93A; acetylglucosamine; carnitine synthesis; fasting; metabolomic GWAS; mitochondrial metabolism; polyamines; solute carrier transporters
    DOI:  https://doi.org/10.1016/j.cmet.2025.09.015
  4. Br J Pharmacol. 2025 Oct 13.
       BACKGROUND AND PURPOSE: Lipolysis is tightly regulated by pro-lipolytic β-adrenoceptor signalling, which activates the cAMP/PKA pathway, and by antilipolytic hormones like insulin and FGF1, which counter-regulate lipolysis through cAMP-degrading phosphodiesterases (PDEs). While the spatial compartmentalization of cAMP signalling is recognized, comparisons between distinct cAMP pools remain under-investigated in adipocytes. Moreover, the dynamics of cAMP around lipid droplets (LD) where lipolysis occurs, are particularly intriguing. Thus, we studied whether adipose FGF1/PDE4D and insulin/PDE3B pathways regulate distinct cAMP microdomains to execute their antilipolytic actions.
    EXPERIMENTAL APPROACH: We evaluated the role of subcellular cAMP pools in lipolysis regulation by PDEs, or antilipolytic hormones, by utilizing EPAC1-based FRET cAMP biosensors specifically designed to localize in the cytoplasm or at the plasma membrane of living cells. Additionally, we developed the first LD-associated cAMP biosensor by fusing the lipid droplet-associated protein perilipin-1 to the EPAC1-based probe.
    KEY RESULTS: We identified previously unrecognized cAMP pools surrounding LDs that are distinct from cytoplasmic cAMP and resistant to PDE inhibition or antilipolytic stimuli. PDE4D exhibits a stronger effect on all three cAMP pools investigated than PDE3B. FGF1 mainly inhibits the cAMP in the initiation of the signalling at the plasma membrane, whereas insulin targets mainly cytoplasmic cAMP pools.
    CONCLUSION AND IMPLICATIONS: The discovery of LD-associated cAMP as a distinct subcellular pool suggests that cAMP signalling in adipocytes is more compartmentalized than previously recognized. The distinct pathways by which FGF1 and insulin regulate adipose cell cAMP levels highlight that antilipolytic signalling is not uniform, refining our understanding of lipolysis regulation.
    Keywords:  FGF1; FRET; PDE3B; PDE4D; cAMP; insulin; lipolysis
    DOI:  https://doi.org/10.1111/bph.70216
  5. Cell Metab. 2025 Oct 16. pii: S1550-4131(25)00394-8. [Epub ahead of print]
      Metabolic dysregulation is a hallmark of aging. Here, we investigate in mice age-induced metabolic alterations using metabolomics and stable isotope tracing. Circulating metabolite fluxes and serum and tissue concentrations were measured in young and old (20-30 months) C57BL/6J mice, with young obese (ob/ob) mice as a comparator. For major circulating metabolites, concentrations changed more with age than fluxes, and fluxes changed more with obesity than with aging. Specifically, glucose, lactate, 3-hydroxybutryate, and many amino acids (but notably not taurine) change significantly in concentration with age. Only glutamine circulatory flux does so. The fluxes of major circulating metabolites remain stable despite underlying metabolic changes. For example, lysine catabolism shifts from the saccharopine toward the pipecolic acid pathway, and both pipecolic acid concentration and flux increase with aging. Other less-abundant metabolites also show coherent, age-induced concentration and flux changes. Thus, while aging leads to widespread metabolic changes, major metabolic fluxes are largely preserved.
    Keywords:  aging; fluxomics; glutamine; metabolic flux; metabolism; metabolomics; obesity; stable isotope tracing; systemic metabolism
    DOI:  https://doi.org/10.1016/j.cmet.2025.09.009
  6. JCI Insight. 2025 Oct 16. pii: e196280. [Epub ahead of print]
      Pancreatic ductal adenocarcinoma (PDAC) is a rapidly metastasizing cancer characterized by a dense desmoplastic stroma comprised of extracellular matrix (ECM) proteins, which complicates treatment. Upon stimulation, pancreatic stellate cells (PSCs) differentiated into cancer-associated fibroblasts (CAFs) that are the source of ECM and cytokines in PDAC. We previously reported that mechanical stress activates PSCs and induces fibrosis through mechanical ion channel PIEZO1-mediated TRPV4 channel activation, but its role in PDAC remains unclear. Here we report that pathological activation of PIEZO1 differentiated human PSCs into an inflammatory CAF phenotype that expresses chemoresistance and cancer stemness markers CD10 and GPR77. In an orthotopic PDAC model, TRPV4 knockout mice exhibited a significant reduction in tumor size, circulating inflammatory cytokines, tissue inhibitor of metalloproteinases-1 (TIMP1), and pre-metastatic niche markers, serum amyloid A (SAA) proteins. A similar trend was observed in mice lacking functional PIEZO1 in PSCs. The livers of TRPV4 knockout mice exhibited fewer cancer cell microlesions, lacked macro tumors, produced lower levels of inflammatory protein S100A8, and developed fewer inflammatory cell clusters. In orthotopic and genetically engineered models of PDAC, these mice also had improved survival, suggesting that blocking TRPV4 channels may be a promising therapeutic target for PDAC.
    Keywords:  Cancer; Fibrosis; Gastroenterology; Ion channels; Oncology
    DOI:  https://doi.org/10.1172/jci.insight.196280
  7. Mol Cancer Res. 2025 Oct 14.
      Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy, associated with early metastasis, drug resistance and poor outcomes. We previously demonstrated a putative tumor suppressive role for concentrative nucleoside transporter 1 (CNT1) in PDAC. Here we demonstrate the regulator of G protein signaling (RGS) 11 as a key target of CNT1, with potent tumor suppressive properties in PDAC. Compared to normal human pancreas, RGS11 expression is diminished in human PDAC tissues which correspond with the reduced patient survival times. In addition, quasi-mesenchymal pancreatic tumor cell lines with accelerated growth, metastatic propensity, and innate resistance to nucleoside analogs showed relatively lower RGS11 expression than the epithelial counterparts. Interestingly, RGS11 levels reversibly modulated the epithelial-mesenchymal transition (EMT) of human PDAC cell lines influencing the chemotherapeutic sensitivities of anti-PDAC drugs. Additionally, stable lentiviral-mediated RGS11 expression reduced the cellular proliferation and colony establishment, increased the apoptotic index, and decreased the migratory and invasive abilities in quasi-mesenchymal tumor cell lines, whereas RGS11 depletion in epithelial tumor cell lines showed opposite effects. Global transcriptomic analysis revealed RGS11 replenishment in PDAC cells to suppress CD44-directed stemness features with significant reprogramming of the PDAC oncogenic landscape. Furthermore, RGS11 reduced the primary tumor burden and metastatic occurrence in a mouse model of PDAC. Together, these findings uncover RGS11 as a key target of CNT1 that exhibits therapeutic potential for intervention of aggressive PDAC. Implications: RGS11 identified as a downstream target of a gemcitabine transporter CNT1 exerts potent anti-tumorigenic features in pancreatic ductal adenocarcinoma with therapeutic and prognostic values.
    DOI:  https://doi.org/10.1158/1541-7786.MCR-25-0144
  8. Nat Commun. 2025 Oct 17. 16(1): 9234
      Lysosomes are essential organelles for cellular homeostasis and signaling, with dysfunction linked to neurological disorders, lysosomal storage diseases, and cancer. While proteomics has advanced our understanding of lysosomal composition, the structural characterization of lysosomal membrane proteins in their native environment remains a significant challenge. Here, we developed a cryo electron tomography workflow to visualize lysosomal membrane proteins within intact, native lysosomal membranes. We isolated endolysosomes by independently targeting two lysosomal membrane proteins, transient receptor potential mucolipin 1 and transmembrane protein 192, enriching organelles that exhibited the expected morphology and proteomic composition of the endolysosomal system. Sub-tomogram averaging enabled the structural refinement of key membrane and membrane-associated proteins, including V-ATPase, Flotillin, and Clathrin, directly within the lysosomal membrane, revealing their heterogeneous distribution across endolysosomal organelles. By integrating proteomics with structural biology, our workflow establishes a powerful platform for studying lysosomal membrane protein function in health and disease, paving the way for future discoveries in membrane-associated lysosomal mechanisms.
    DOI:  https://doi.org/10.1038/s41467-025-64314-0
  9. Sci Adv. 2025 Oct 17. 11(42): eadx0632
      Analyses of patient-derived cell lines have greatly enhanced discovery of molecular biomarkers and therapeutic targets. However, characterization of cellular morphological properties is limited. We studied cell morphologies of human pancreatic adenocarcinoma (PDAC) cell lines and their associations with drug sensitivity, gene expression, and functional properties. By integrating live cell and spatial messenger RNA imaging, we identified KRAS inhibitor-induced morphological changes specific for drug-resistant cells that correlated with gene expression changes. We then categorized a large panel of patient-derived PDAC cell lines into morphological and organizational subtypes and found differences in gene expression, therapeutic targeting potential, and metastatic proclivity. Patterns of cancer cell organization in human PDAC tissues stratified distinct gene expression signatures with clinical significance. In summary, we highlight the potential of cell morphological information in rapid, cost-effective assays to aid precision oncology efforts leveraging patient-derived in vitro models and tissues.
    DOI:  https://doi.org/10.1126/sciadv.adx0632
  10. Cancer Res. 2025 Oct 17.
      Pancreatic cancer is associated with a high rate of metastasis and poor prognosis. The formation of a premetastatic niche (PMN) facilitates cancer cell spread and contributes to cancer mortality. Using murine pancreatic cancer models based on expression of oncogenic KRAS in the pancreas epithelium, we discovered that remodeling of the lung microenvironment occurred in mice bearing pancreatic precursor lesions prior to cancer formation. This early lesion premetastatic niche (EL-PMN) resembled the PMN in cancer-bearing mice, and both feature characteristics of overt metastasis, such as transcriptional reprogramming, activation of fibroblast STAT3 signaling, and infiltration of immunosuppressive ARG1+ macrophages. Both pancreatic cancer patients and mouse models demonstrated elevated serum IL6. Inactivating oncogenic KRAS reduced serum IL6 and reverted fibroblast STAT3 phosphorylation in mouse lungs; loss of lung fibroblast STAT3 phosphorylation was similarly observed when mice were treated with the pan-RAS inhibitor RMC7977. While ARG1+ macrophage infiltration was dispensable for fibroblast STAT3 activation, IL6 blockade inhibited lung fibroblast STAT3 activation. Functionally, fibroblast STAT3 activation was necessary for lung metastasis establishment and growth. Interestingly, activation of STAT3 in the PMN was present in the lungs but not in the liver, where fibroblast reprogramming occurred only in overt metastasis, pointing to organ-specific PMN formation. In human metastasis samples, phosphorylated STAT3 in fibroblasts was similarly more abundant in the lungs than liver. Together, these data point to organ-specific mechanisms driving formation of the PMN and indicate that reprogramming of the microenvironment prior to metastasis might support early dissemination of pancreatic cancer.
    DOI:  https://doi.org/10.1158/0008-5472.CAN-25-3472
  11. ACS Biomater Sci Eng. 2025 Oct 11.
      Conventional cell culture substrates are flat and rigid, locking cells in a permanent and unphysiological geometry. Advanced tissue culture models that emulate the dynamic and 3D environments of organs remain challenging to generate. Here, we establish flexible silicone adhesive films as versatile substrates that enable the on-demand release, transfer, and folding of cultured 2D tissues into 3D geometries. We rolled primary epithelial cultures into tubes, assembled cuboidal structures, and transferred primary endothelial cultures between culture environments for coculturing. Our approach provides an easy-to-implement platform for dynamic geometrical designs in tissue engineering.
    Keywords:  3D; adhesives; flexible tissue engineering; foldable; low-cost technology; primary cell cultures
    DOI:  https://doi.org/10.1021/acsbiomaterials.5c01130
  12. Methods Mol Biol. 2026 ;2976 85-102
      Lysosomes, known for degrading biomolecules and damaged cellular components, are now recognized as signaling hubs for nutrient sensing and metabolic adaptation, and their dysfunction is implicated in diseases including cancer and neurodegeneration. To understand the composition of the lysosome, the dynamic behavior of its contents, and its specific roles in health and disease, we describe a lysosomal immunoprecipitation method, termed "LysoIP," that enables the isolation of intact lysosomes from cultured cells and mouse tissues. This method utilizes a lysosome-localized 3xHA epitope tag (LysoTag) and a simple, yet robust organelle immunoprecipitation workflow. Isolated lysosomes are extracted with optimized buffers to allow the efficient retrieval of lysosomal proteins, polar metabolites, and lipids, maintaining compatibility with downstream liquid chromatography and mass spectrometry (LC-MS) analyses.
    Keywords:  LC-MS analyses; LysoIP; LysoTag; LysoTag mouse; Lysosomes; Metabolomics; Proteomics; TMEM192
    DOI:  https://doi.org/10.1007/978-1-0716-4844-5_8
  13. Aging Cell. 2025 Oct 13. e70246
      Autophagy is intricately linked with protective cellular processes, including mitochondrial function, proteostasis, and cellular senescence. Animal studies have indicated that autophagy becomes dysfunctional with aging and may contribute to T cell immunosenescence. In humans, it remains unclear whether autophagy is impaired in CD4+ T cells as people age. To answer this question, we examined basal and inducible autophagic activity in a series of experiments comparing CD4+ T cells from younger (23-35 years old) and older (67-93 years old) healthy donors. We used immunofluorescence to detect LC3 (a marker of autophagosomes and autolysosomes) and LAMP2 (a marker of endolysosomes) in conjunction with bafilomycin A1 (which inhibits the acidification of lysosomes) and CCCP (a mitochondrial uncoupler) to manipulate autophagic flux. We found a significantly higher autophagy flux in CD4+ T cells from older compared to younger donors and a higher number of LC3+ compartments among older donors. Since the overall amount of autophagosomes degraded was comparable between the two groups, we concluded that autophagosome biogenesis was reduced in the older group. Rather than a decline, our findings in healthy older donors point toward a compensatory enhancement of human CD4+ T cell autophagy with age, which may be a mechanism behind healthy aging.
    Keywords:  CD4+ T cells; autophagy; healthy aging
    DOI:  https://doi.org/10.1111/acel.70246
  14. Proc Natl Acad Sci U S A. 2025 Oct 21. 122(42): e2512977122
      Understanding how bacteria interact with surfaces is critical for advancing applications in biofilm and biofouling prevention, biomaterial development, or biosensing. However, the biophysical mechanisms underlying these interactions remain poorly characterized, and novel microscopy strategies are needed to specifically address the biointerface. In this study, we employ fluorescence lifetime imaging microscopy (FLIM) with the tension reporter Flipper-TR to investigate membrane tension in live bacteria interacting with various surfaces. We show that Flipper-TR stains both Gram-positive and Gram-negative bacterial membranes, exhibiting fluorescence lifetimes shorter than those in eukaryotic cells, with slight variations between bacterial types and likely reflecting differences in membrane composition. Flipper-TR displays lifetime variations along the vertical axis of bacterial cells, suggesting spatial differences in membrane tension influenced by cell wall architecture. Our results further demonstrate that Flipper-TR is responsive to the nature of bacterial interactions with surfaces. By comparing bacterial immobilization on surfaces with different coatings, we show that Flipper-TR can sensitively distinguish differences in membrane tension arising from distinct adhesion mechanisms. Additionally, Flipper-TR detects changes in membrane tension when bacteria are exposed to engineered nanostructured substrates. Overall, this work expands the toolbox to study the mechanical aspects of bacterial-material interactions and contributes to providing design rules for novel materials that influence bacterial behavior.
    Keywords:  bacteria; cell–material interface; fluorescence lifetime imaging; membrane tension probe; nanotopographies
    DOI:  https://doi.org/10.1073/pnas.2512977122
  15. Bio Protoc. 2025 Oct 05. 15(19): e5455
      Rapid and uniform labeling of plasma membrane proteins is essential for high-resolution imaging of dynamic membrane topologies and intercellular communication in live mammalian cells. Existing strategies for labeling live cell membranes, such as fluorescent fusion proteins, enzyme-mediated tags, metabolic bioorthogonal labeling, and lipophilic dyes, face trade-offs in the requirement of genetic manipulation, the presence of non-uniform labeling, the need for extensive preparation times, and limited choices of fluorophores. Here, we present a streamlined protocol that leverages N-hydroxysuccinimide (NHS)-ester chemistry to achieve rapid (≤5 min), covalent conjugation of synthetic small-molecule dyes to surface-exposed primary amines, enabling pan-membrane-protein labeling. This workflow covers dye stock preparation, labeling for suspension and adherent cells, multiplex live-cell imaging, fusion protein co-staining (including insulin-triggered receptor endocytosis), 3D membrane visualization, and in vivo assays for visualizing membrane-derived material transfers between donor and recipient cells using a lymphoma T-cell mouse model. This high-density labeling approach is compatible with various cell types across diverse imaging platforms. Its speed, versatility, and stability make it a broadly applicable tool for studying plasma membrane dynamics and intercellular membrane trafficking. Key features • Rapid high-density membrane labeling with small-molecule fluorescent dyes. • Enables live-cell multiplexed imaging, amenable to primary cells and cells expressing fluorescent fusion proteins, and supports in vivo studies of membrane-associated cell-cell communications. • Compatible with various fluorescence imaging modalities.
    Keywords:  Cell–cell communication; Covalent protein labeling; Live-cell imaging; NHS-ester labeling; Plasma membrane
    DOI:  https://doi.org/10.21769/BioProtoc.5455
  16. Bioinformatics. 2025 Oct 16. pii: btaf571. [Epub ahead of print]
       SUMMARY: Whereas transcriptomic and spatial profiling offer static snapshots of tissue structure, mechanistic models use biological rules to predict how tissues evolve. We present the BioInformatics WalkThrough (BIWT) software to directly initialize spatial agent-based models (ABMs) from single-cell and spatial molecular data. We demonstrate how initialization strategies affect tumor-immune dynamics and spatial clustering, positioning BIWT as a software suite to generate data-driven virtual cells representing both experimental and clinical contexts.
    AVAILABILITY AND IMPLEMENTATION: The BIWT software is available at https://github.com/PhysiCell-Tools/PhysiCell-Studio. The sample dataset for running the BIWT is available at https://zenodo.org/records/16365625. The code and instructions for reproducing the use case example is available at https://github.com/drbergman/BIWT-Paper.
    SUPPLEMENTARY INFORMATION: The online supplementary link will be placed here when it is finalized.
    Keywords:  agent-based model; multiomics; predictive modeling; spatial multiomics; virtual cells
    DOI:  https://doi.org/10.1093/bioinformatics/btaf571
  17. Nature. 2025 Oct 15.
      All mammalian organs depend on resident macrophage populations to coordinate repair and facilitate tissue-specific functions1-3. Functionally distinct macrophage populations reside in discrete tissue niches and are replenished through a combination of local proliferation and monocyte recruitment4,5. Declines in macrophage abundance and function have been linked to age-associated pathologies, including atherosclerosis, cancer and neurodegeneration6-8. However, the mechanisms that coordinate macrophage organization and replenishment within ageing tissues remain largely unclear. Here we show that capillary-associated macrophages (CAMs) are selectively lost over time, contributing to impaired vascular repair and reduced tissue perfusion in older mice. To investigate resident macrophage behaviour in vivo, we used intravital two-photon microscopy in live mice to non-invasively image the skin capillary plexus, a spatially well-defined vascular niche that undergoes rarefication and functional decline with age. We find that CAMs are lost at a rate exceeding capillary loss, resulting in macrophage-deficient vascular niches in both mice and humans. CAM phagocytic activity was locally required to repair obstructed capillary blood flow, leaving macrophage-deficient niches selectively vulnerable under homeostatic and injury conditions. Our study demonstrates that homeostatic renewal of resident macrophages is less precisely regulated than previously suggested9-11. Specifically, neighbouring macrophages do not proliferate or reorganize to compensate for macrophage loss without injury or increased growth factors, such as colony-stimulating factor 1 (CSF1). These limitations in macrophage renewal may represent early and targetable contributors to tissue ageing.
    DOI:  https://doi.org/10.1038/s41586-025-09639-y
  18. Elife. 2025 Oct 15. pii: RP102097. [Epub ahead of print]13
      Intravital microscopy (IVM) enables live imaging of animals at single-cell level, offering essential insights into cancer progression. This technique allows for the observation of single-cell behaviors within their natural 3D tissue environments, shedding light on how genetic and microenvironmental changes influence the complex dynamics of tumors. IVM generates highly complex datasets that often exceed the analytical capacity of traditional uni-parametric approaches, which can neglect single-cell heterogeneous in vivo behavior and limit insights into microenvironmental influences on cellular behavior. To overcome these limitations, we present BEHAV3D Tumor Profiler (BEHAV3D-TP), a computational framework that enables unbiased single-cell classification based on a range of morphological, environmental, and dynamic single-cell features. BEHAV3D-TP integrates with widely used 2D and 3D image processing pipelines, enabling researchers without advanced computational expertise to profile cancer and healthy cell dynamics in IVM data from mouse models. Here, we apply BEHAV3D-TP to study diffuse midline glioma (DMG), a highly aggressive pediatric brain tumor characterized by invasive progression. By extending BEHAV3D-TP to incorporate tumor microenvironment (TME) data from IVM or fixed correlative imaging, we demonstrate that distinct migratory behaviors of DMG cells are associated with specific TME components, including tumor-associated macrophages and vasculature. BEHAV3D-TP enhances the accessibility of computational tools for analyzing the complex behaviors of cancer cells and their interactions with the TME in IVM data.
    Keywords:  cancer biology; cell migration; computational biology; confocal microscopy; image analysis; mouse; systems biology
    DOI:  https://doi.org/10.7554/eLife.102097
  19. Nat Med. 2025 Oct 16.
      End-of-life events related to carcinoma lethality are poorly characterized. Herein we conducted an observational, prospective, case-control study enrolling 21 patients with solid tumors and 10 patients without known malignancy, complemented by a retrospective validation cohort of 1,250 patients with cancer. In our prospective cohort, we observed spikes in circulating tumor cell (CTC) counts, particularly clusters, immediately before death (P < 0.0001), as well as pathological evidence of macrovascular infiltration and large-vessel occlusion obtained through rapid autopsy. In the validation cohort, radiological evidence of macrovascular infiltration emerged as the strongest predictor of poor survival-independent of metastasis-in treatment-homogeneous patients with colorectal, lung, ovarian, hepatocellular or pancreatic cancer (hazard ratios = 4.0-22.4). Collectively, these findings suggest that macrovascular infiltration and spikes in CTC clusters with consequent vascular failure could be pivotal end-of-life events associated with cancer lethality, providing a rationale for future trials aimed at curbing infiltration into large vessels.
    DOI:  https://doi.org/10.1038/s41591-025-03966-3
  20. BMC Cancer. 2025 Oct 14. 25(1): 1572
       BACKGROUND: Cachexia is a major challenge throughout cancer treatment. Unintentional weight loss, the principal diagnostic criterium of cancer cachexia, is usually assessed through self-reported body weight change, which may be prone to bias. Other aspects of cancer cachexia include altered body composition (e.g., loss of muscle mass) and impaired physical activity. The central aim of the 'Patient-Recorded Indexing MeasurementS' (PRIMS) study is to improve the accuracy of the diagnosis of cachexia in patients with cancer. The primary objectives are to compare self-reported and objectively measured pre-treatment weight changes, and to assess their respective association with treatment-related adverse events and survival. Secondary objectives are to define host phenotypes based on combinations of objectively assessed cachexia-related data that are predictive of treatment-related adverse events and survival, and to investigate longitudinal associations between body weight and physical activity patterns.
    METHODS: This prospective observational cohort study will be conducted in two Dutch referral centers specialized in treatment of patients with upper gastrointestinal, hepatobiliary, pancreatic, colorectal, and ovarian cancer. We will include 300 cancer patients scheduled for either neoadjuvant chemo(radio)therapy or upfront elective surgery. Patients will undergo a baseline assessment consisting of nutritional screening (anthropometry, body weight assessment), body composition analysis, and physical fitness tests. Patients will be provided with an accelerometer and weight scale for continuous/daily at-home measurements before, throughout, and after treatment. Treatment-related adverse events will be assessed according to the Common Terminology Criteria for Adverse Events or Clavien-Dindo classification. Response to chemo(radio)therapy will be assessed according to 'Response Evaluation Criteria in Solid Tumors' (RECIST) criteria. Disease-free and overall survival will be recorded. Relationships between cachexia-related parameters and outcomes will be investigated using multivariable logistic regression analysis.
    DISCUSSION: The PRIMS protocol comprises a core assessment set of objective measurements to improve the diagnosis of cancer cachexia. It will help to identify patient phenotypes associated with treatment-related adverse events and survival. This approach is expected to advance cachexia diagnostics and enhance future clinical and translational research on the prevalence, severity, and impact of cancer cachexia. PRIMS will also aid clinicians in providing personalized counseling on treatment options and their expected outcomes.
    TRIAL REGISTRATION: Medical Ethics Committee of the Academic Hospital Maastricht/Maastricht University (azM/UM) (METC18012, version 4.0, June 2024), Netherlands Trial Register (NL65402.068.18). The trial is registered in the ClinicalTrials.gov register (NCT05899205).
    Keywords:  Body weight change; Cancer cachexia; Physical activity; Physical fitness
    DOI:  https://doi.org/10.1186/s12885-025-14979-z
  21. Methods Mol Biol. 2026 ;2976 47-60
      Autophagy is a conserved lysosomal degradation pathway that recycles protein aggregates and damaged organelles to maintain cytoplasmic quality control. Measuring the amount of the lipid-conjugated autophagic protein LC3B-II is a useful way to test whether a particular perturbation affects autophagy. However, the level of LC3B-II is affected by factors that alter either the rate of autophagosome biogenesis or degradation. Consequently, the same steady-state LC3B-II level can be reached by opposing autophagic fluxes. It is thus essential when measuring LC3B-II to perform the assay both in the absence and presence of a lysosomal inhibitor, enabling measurement of the rate of synthesis independent of its degradation. LC3B-II is also a small protein that can be challenging to detect by western blotting. In this chapter, we will provide a method for the efficient western blotting of LC3B-II and guidance as to the interpretation of the results.
    Keywords:  ATG8; Autophagy; Bafilomycin A1; LC3B; SDS-PAGE; Western blotting
    DOI:  https://doi.org/10.1007/978-1-0716-4844-5_5
  22. Biophys J. 2025 Oct 13. pii: S0006-3495(25)00666-6. [Epub ahead of print]
      Membrane integrity under chemical stress is critical to cellular survival and industrial microbial bioproduct formation, yet the molecular determinants that govern bilayer resilience remain incompletely understood. Here, we use all-atom molecular dynamics simulation to compare the biophysical responses to increasing concentrations of 1-butanol membranes comprised of unbranched, saturated (1,2-dipalmitoyl-sn-glycero-3-phosphocholine, DPPC) and branched, saturated (1-anteiso-palmitoyl-2-palmitoyl-sn-glycero-3-phosphocholine, APPC) lipids. These two lipids differ by a single methyl group attached to the APPC system. In the absence of butanol, both membranes exhibit well-ordered architectures consistent with experimental benchmarks; however, under increasing solvent stress, their behaviors diverge markedly. DPPC membranes display gradual thinning, modest area per lipid (APL) expansion, and sustained acyl chain order, resulting in only moderate declines in bending rigidity and lateral mobility. In contrast, APPC bilayers exhibit accelerated thinning, pronounced lateral expansion, and significant loss of chain order, culminating in enhanced interleaflet overlap and a sharp decline in bending modulus, reflecting a fundamental breakdown of bilayer symmetry and mechanical resistance. Together, our findings reveal how lipid tail architecture modulates membrane vulnerability to organic solvents and suggest that branching, while potentially beneficial under thermal stress, renders membranes more susceptible to solvent-induced collapse.
    DOI:  https://doi.org/10.1016/j.bpj.2025.10.015
  23. Spectrochim Acta A Mol Biomol Spectrosc. 2025 Oct 10. pii: S1386-1425(25)01338-1. [Epub ahead of print]347 127031
      Lipid droplets (LDs) are spherical organelles that play critical roles in various physiological and pathological metabolic processes and hold potential as diagnostic markers for cancer. Therefore, the precise localization and monitoring of LDs are crucial for medical research and health care, making fluorescent probes with high sensitivity and specificity particularly valuable for bioimaging and tumor diagnosis. In this study, leveraging the highly viscous microenvironment of LDs, we designed and synthesized two fluorescent probes, referred to as TPA-LDs which exhibit aggregation-induced emission (AIE) characteristics. Among these, TPA-LD1 demonstrated excited state intramolecular proton transfer (ESIPT) properties. The ESIPT-favorable environment aligns well with the conditions that support LDs viability, thereby enabling TPA-LD1 to promote the occurrence of the ESIPT process under the condition of specifically and effectively targeting LDs. In cellular imaging applications, the TPA-LD1 probe effectively highlighted changes in LDs quantity in cells during oleic acid accumulation and facilitated the distinction between cancerous and normal cells.
    Keywords:  Aggregation-induced emission; Fluorescent probe; Lipid droplet (LDs) imaging; Viscosity
    DOI:  https://doi.org/10.1016/j.saa.2025.127031
  24. Nat Phys. 2025 ;21(10): 1629-1637
      Many physiological processes, such as the shear flow alignment of endothelial cells in the vasculature, depend on the transition of cell layers between disordered and ordered phases. Here we demonstrate that such a transition is driven by the non-monotonic evolution of nematic topological defects in a layer of endothelial cells and the emergence of string excitations that bind the defects together. This suggests the existence of an intermediate phase of ordering kinetics in biological matter. We use time-resolved large-scale imaging and physical modelling to analyse the non-monotonic decrease in the number of defect pairs. The interaction of the intrinsic cell layer activity and the alignment field determines the occurrence of defect domains, which defines the nature of the transition. Defect pair annihilation is mediated by string excitations spanning multicellular scales within the cell layer. Our results, therefore, suggest a mechanism by which intermediate ordering and string excitation might contribute to regulating morphogenetic movements and tissue remodelling in vivo.
    Keywords:  Biological physics; Topological defects
    DOI:  https://doi.org/10.1038/s41567-025-03014-4
  25. Cell Death Discov. 2025 Oct 16. 11(1): 465
      FOXO transcription factors act downstream of PI3K signaling, and FOXO transcriptional activity is inhibited through nuclear exclusion by PKB/AKT-mediated phosphorylation. Many studies have shown FOXO to contribute to organismal homeostasis by mitigating (extra)cellular stress to prevent cell death (reviewed in [1]). Here we show that FOXO3 activation protects cells from ferroptosis, an iron-dependent form of non-apoptotic cell death. In untransformed hTERT-RPE-1 cells, FOXO3 activation reduces ferroptosis in a multilayered manner. First, FOXO3 mediates protection from ferroptosis in part through a p27-induced G1 cell cycle arrest. Second, FOXO3 activation reduces cellular H2O2 levels, thereby limiting substrate availability for the Fenton reaction, which fuels hydroxyl radical formation for lipid peroxidation. Third, FOXO3 activation lowers cellular iron content by reducing TFR1 expression, which, combined with the lowering of cellular H2O2 levels, likely further reduces the formation of hydroxyl radicals through the Fenton reaction. Finally, FOXO3 activation reduces expression of long-chain-fatty-acid-CoA ligase 4 (ACSL4) and Peroxisomal targeting signal 1 receptor (PEX5), proteins involved in lipid metabolism and protection against ferroptosis. Taken together, we show that FOXO3 activation results in protection from ferroptosis, adding to the repertoire of FOXO-controlled cell protection programs.
    DOI:  https://doi.org/10.1038/s41420-025-02760-x
  26. Methods Mol Biol. 2026 ;2976 35-45
      Photothermal microscopy is an optical imaging technique used to visualize the distribution of trace amounts of endogenous dyes in living cells. This technique facilitates lysosomal observation and functional analysis by detecting and identifying accumulated substances within them, eliminating the need for molecular labeling. Here, we describe the fundamental principles and system configuration of a photothermal microscope. We also present a detailed procedure for performing photothermal measurements in living cells.
    Keywords:  Autophagy; Label-free; Live-cell imaging; Optical absorption; Photothermal microscope
    DOI:  https://doi.org/10.1007/978-1-0716-4844-5_4
  27. FEBS J. 2025 Oct 17.
      Developing techniques to visualize intracellular structures, which influence the spatiotemporal functionality of biomolecules, is essential for elucidating mechanisms governing cellular behavior. In this study, we demonstrate that label-free external apodized phase-contrast (ExAPC) microscopy serves as a valuable tool for the simultaneous observation of various intracellular structures with high spatiotemporal resolution, while successfully mitigating halo artifacts. Additionally, through quantitative analysis of images obtained by combining ExAPC microscopy with fluorescence microscopy, we identified distinct heterogeneities in biomolecular condensates, lipid droplets, and mitochondria. Our findings highlight the potential of ExAPC microscopy to provide detailed insights into alterations in intracellular structures associated with diverse cellular processes, corroborating the existing knowledge and potentially contributing to the discovery of previously unknown cellular mechanisms.
    Keywords:  biomolecular condensates; cellular organization; external apodization phase‐contrast microscopy; lipid droplets; mitochondria dynamics
    DOI:  https://doi.org/10.1111/febs.70286
  28. Mol Cell. 2025 Oct 13. pii: S1097-2765(25)00781-6. [Epub ahead of print]
      Protein arginine methyltransferase 5 (PRMT5) catalyzes symmetric arginine dimethylation (Rme2s) of RNA-binding proteins and influences RNA splicing and gene expression. However, how PRMT5 couples splicing to productive transcript output remains unclear. We show that a major function of PRMT5 is to promote chromatin escape of mRNAs, designated as genomically retained incompletely processed polyadenylated transcripts (GRIPPs). Using nascent and spike-in normalized fractionated transcriptomics with proteomics, we find that PRMT5 inhibition in mammalian cells causes polyadenylated mRNA and Smith antigen (Sm) protein accumulation on chromatin. These retained transcripts are intron rich and splice slowly. PRMT5 inhibition and isogenic SNRPB mutants demonstrate that Sm tail methylation is essential to prevent RNA detention on chromatin. Biochemical assays reveal that the SMN Tudor domain competes with nucleic acid binding of methylated Sm tails. We conclude that PRMT5 ensures mRNA processing and nuclear export by preventing aberrant chromatin retention, highlighting arginine methylation as a key regulator of RNA-chromatin dynamics.
    Keywords:  CLNS1A; PRMT5; RIOK1; Rme2s; SDMA; SMN; SNRPB; SNRPD1; SNRPD3; pICln
    DOI:  https://doi.org/10.1016/j.molcel.2025.09.021
  29. Int J Mol Sci. 2025 Sep 23. pii: 9261. [Epub ahead of print]26(19):
      Insights into the state of individual cells within a living organism are essential for identifying diseases and abnormalities. The internal state of a cell is reflected in its morphological features and changes in the localization of intracellular molecules. Using this information, it is possible to infer the state of the cells with high precision. In recent years, technological advancements and improvements in instrument specifications have made large-scale analyses, such as single-cell analysis, more widely accessible. Among these technologies, imaging flow cytometry (IFC) is a high-throughput imaging platform that can simultaneously acquire information from flow cytometry (FCM) and cellular images. While conventional FCM can only obtain fluorescence intensity information corresponding to each detector, IFC can acquire multidimensional information, including cellular morphology and the spatial arrangement of proteins, nucleic acids, and organelles for each imaging channel. This enables the discrimination of cell types and states based on the localization of proteins and organelles, which is difficult to assess accurately using conventional FCM. Because IFC can acquire a large number of single-cell morphological images in a short time, it is well suited for automated classification using machine learning. Furthermore, commercial instruments that combine integrated imaging and cell sorting capabilities have recently become available, enabling the sorting of cells based on their image information. In this review, we specifically highlight practical applications of IFC in four representative areas: cell cycle analysis, protein localization analysis, immunological synapse formation, and the detection of leukemic cells. In addition, particular emphasis is placed on applications that directly contribute to elucidating molecular mechanisms, thereby distinguishing this review from previous general overviews of IFC. IFC enables the estimation of cell cycle phases from large numbers of acquired cellular images using machine learning, thereby allowing more precise cell cycle analysis. Moreover, IFC has been applied to investigate intracellular survival and differentiation signals triggered by external stimuli, to monitor DNA damage responses such as γH2AX foci formation, and more recently, to detect immune synapse formation among interacting cells within large populations and to analyze these interactions at the molecular level. In hematological malignancies, IFC combined with fluorescence in situ hybridization (FISH) enables high-throughput detection of chromosomal abnormalities, such as BCR-ABL1 translocations. These advances demonstrate that IFC provides not only morphological and functional insights but also clinically relevant genomic information at the single-cell level. By summarizing these unique applications, this review aims to complement existing publications and provide researchers with practical insights into how IFC can be implemented in both basic and translational research.
    Keywords:  cell cycle; imaging flow cytometry; immunological synapse; machine learning; protein localization; signal transduction
    DOI:  https://doi.org/10.3390/ijms26199261
  30. Nat Commun. 2025 Oct 15. 16(1): 9130
      Demand for mass spectrometry imaging (MSI) technologies offering subcellular resolution for tissues and cell imaging is rapidly increasing. To accomplish this, efficient analyte ionisation is essential, given the small amounts of sample material in each pixel. Herein, we describe an atmospheric pressure transmission-geometry matrix-assisted laser desorption source equipped with plasma ionisation. By utilising a pre-staining method for sample preparation, lipid signal intensities were enhanced by an order of magnitude compared to conventional matrix-only methods, while serendipitously enabling imaging of numerous nucleotides. The system enables detection of up to 200 lipids and nucleotides in tissues at 1 µm-pixel size while informative MSI data is still obtained down to 250 nm pixel size. The use of sub-micron pixels is shown to discern subcellular features through combinations with fluorescence microscopy. This method provides a powerful tool for cellular and sub-cellular imaging of small molecules from tissues and cells for spatial biology applications.
    DOI:  https://doi.org/10.1038/s41467-025-64604-7
  31. J Physiol. 2025 Oct 16.
      Iron is a biologically indispensable yet potentially harmful element: essential for numerous metabolic processes but toxic in excess, potentially leading to organ damage. Under conditions of extreme physical inactivity, such as microgravity or prolonged bed-rest, physical deconditioning occurs, adversely affecting functional capacities and health. Anaemia and muscle atrophy may contribute to systemic iron redistribution, as red blood cells and skeletal muscle collectively concentrate most body iron. Here we summarize a decade of research conducted in rodent and human ground-based models to investigate how extreme physical inactivity alters systemic and cellular iron homeostasis, and explore the underlying mechanisms. During the first days an increase in plasma iron availability occurs in both men and premenopausal women, likely due to accelerated erythrophagocytosis in spleen and redistribution of iron from degraded erythrocytes. Despite the rapid onset of muscle fibre atrophy under these conditions, skeletal muscle appears to accumulate iron rather than release it and therefore may not necessarily contribute to the systemic redistribution of iron. Increased circulating hepcidin levels observed during this early phase could contribute to both redistribution and tissue iron sequestration. After several weeks of exposure plasma iron availability remains elevated in men exposed to extreme physical inactivity, potentially exposing to chronic tissue iron accumulation. In contrast a return to baseline seems to occur in premenopausal women. These findings point to a broad and persistent redistribution of iron metabolism in men in response to extreme physical inactivity. However the long-term effects on iron metabolism in women remain poorly understood and warrant further investigation.
    Keywords:  disuse; haemoglobin; skeletal muscle; spaceflight; trace elements
    DOI:  https://doi.org/10.1113/JP289149
  32. Nature. 2025 Oct 15.
      The properties of mammalian cells depend on their location within organs. Gene expression in the liver varies between periportal and pericentral hepatocytes1-3, and in the intestine from crypts to villus tips4,5. A key element of tissue spatial organization is probably metabolic, but direct assessments of spatial metabolism remain limited. Here we map spatial metabolic gradients in the mouse liver and intestine. We develop an integrated experimental-computational workflow using matrix-assisted laser desorption/ionization (MALDI) imaging mass spectrometry (IMS), isotope tracing and deep-learning artificial intelligence. Most measured metabolites (>90%) showed significant spatial concentration gradients in the liver lobules and intestinal villi. In the liver, tricarboxylic acid (TCA)-cycle metabolites and their isotope labelling from both glutamine and lactate localized periportally. Energy-stress metabolites, including adenosine monophosphate (AMP), also localized periportally, consistent with a high periportal energy demand. In the intestine, the TCA intermediates malate (tip) and citrate (crypt) showed opposite spatial patterns, aligning with higher glutamine catabolism in tips and lactate oxidation in crypts based on isotope tracing. Finally, we mapped the fate of the obesogenic dietary sugar fructose. In the intestine, oral fructose was catabolized faster in the villus bottom than in the tips. In the liver, fructose-derived carbon accumulated pericentrally as fructose-1-phosphate and triggered pericentral adenosine triphosphate (ATP) depletion. Thus, we both provide foundational knowledge regarding intestine and liver metabolic organization and identify fructose-induced focal derangements in liver metabolism.
    DOI:  https://doi.org/10.1038/s41586-025-09616-5
  33. Methods Cell Biol. 2025 ;pii: S0091-679X(25)00087-1. [Epub ahead of print]199 63-90
      The tumor microenvironment (TME) plays a pivotal role in tumor development, influencing interactions with immune cells, tumor progression, and responses to treatment. Understanding the heterogeneity of the TME is essential for uncovering the mechanisms underlying cell-to-cell interactions and their contribution to tumor dynamics. Recent advancements in high-dimensional imaging technologies, such as multiplex immunofluorescence imaging, imaging mass cytometry (IMC), and multiplexed ion beam imaging (MIBI), have provided powerful tools to investigate the complexity of the TME. These technologies allow for the simultaneous analysis of multiple cellular markers and spatial organization of cells within tissue samples, offering detailed insights into the composition and dynamics of the TME. Specifically, IMC offers a unique advantage by enabling the detection of over 40 proteins in a single tissue slide, facilitating a deeper understanding of cellular interactions in situ, at high resolution, and with minimal interchannel crosstalk. Here, we present the analysis approaches and tools developed for imaging mass cytometry data to unravel cellular composition, spatial organization, and interactions within the TME. These methods aim to enhance our understanding of the intricate interplay between cancer cells, immune cells, and stromal components, ultimately supporting the development of more effective therapeutic strategies.
    Keywords:  Cell-to-cell interactions; High-dimensional imaging; Imaging CyTOF; Imaging mass cytometry (IMC); Spatial analysis; Tumor microenvironment (TME); Tumor-immune contexture
    DOI:  https://doi.org/10.1016/bs.mcb.2025.03.006
  34. J Cell Sci. 2025 Oct 01. pii: jcs263874. [Epub ahead of print]138(19):
      Mechanobiology has demonstrated that precise control over mechanical properties at the whole-cell level is crucial for many biological functions. However, comparatively little attention has been paid to intracellular mechanical properties. Only recently have experimental tools become available to adequately measure the viscoelasticity and mechanical activity of the cytosol, revealing that the active, non-equilibrium nature of the intracellular environment must be carefully considered. To explore the interplay between active forces and viscoelastic properties, it is helpful to consider our current understanding of intracellular active mechanics. In this Review, we aim not only to provide an intuitive and quantitative introduction to the relevant physical concepts, but also to offer an overview of the proteins that establish intracellular active mechanics, highlighting their spatial and temporal variation with a particular focus on the role of mechanical activity, in the form of forces used for enhancing both directed and random transport. Although we are only beginning to uncover the importance of intracellular active mechanics for cellular mechanisms, it is becoming increasingly clear that these properties must be precisely regulated to ensure proper cellular function.
    Keywords:  Active diffusion; Biophysics; Cytoskeleton; Development; Intracellular mechanics; Spatial variation
    DOI:  https://doi.org/10.1242/jcs.263874
  35. Nat Cell Biol. 2025 Oct;27(10): 1688-1707
      Chaperone-mediated autophagy (CMA) declines in ageing and neurodegenerative diseases. Loss of CMA in neurons leads to neurodegeneration and behavioural changes in mice but the role of CMA in neuronal physiology is largely unknown. Here we show that CMA deficiency causes neuronal hyperactivity, increased seizure susceptibility and disrupted calcium homeostasis. Pre-synaptic neurotransmitter release and NMDA receptor-mediated transmission were enhanced in CMA-deficient females, whereas males exhibited elevated post-synaptic AMPA-receptor activity. Comparative quantitative proteomics revealed sexual dimorphism in the synaptic proteins degraded by CMA, with preferential remodelling of the pre-synaptic proteome in females and the post-synaptic proteome in males. We demonstrate that genetic or pharmacological CMA activation in old mice and an Alzheimer's disease mouse model restores synaptic protein levels, reduces neuronal hyperexcitability and seizure susceptibility, and normalizes neurotransmission. Our findings unveil a role for CMA in regulating neuronal excitability and highlight this pathway as a potential target for mitigating age-related neuronal decline.
    DOI:  https://doi.org/10.1038/s41556-025-01771-1
  36. Mol Cell. 2025 Oct 10. pii: S1097-2765(25)00703-8. [Epub ahead of print]
      Methylated amino acids accumulate upon the degradation of methylated proteins and are implicated in diverse metabolic and signaling pathways. Disturbed methylated amino acid homeostasis is associated with cardiovascular disease and renal failure. Mitochondria are core processing hubs in conventional amino acid metabolism, but how they interact with methylated amino acids is unclear. Here, we reveal that the orphan mitochondrial solute carrier 25A45 (SLC25A45) is required for the mitochondrial uptake of methylated amino acids. SLC25A45 binds with dimethylarginine and trimethyllysine but has no affinity for unmethylated arginine and lysine. A non-synonymous mutation of human SLC25A45 (R285C) stabilizes the carrier by limiting its proteolytic degradation and associates with altered methylated amino acids in human plasma. Metabolic tracing of trimethyllysine in cancer cells demonstrates that SLC25A45 drives the biosynthesis of the key amino acid derivative, carnitine. SLC25A45 is therefore an essential mediator of compartmentalized methylated amino acid metabolism.
    Keywords:  SLC25; carnitine; metabolism; metabolite transport; methylated amino acids; mitochondria; solute carriers
    DOI:  https://doi.org/10.1016/j.molcel.2025.08.018
  37. EMBO Rep. 2025 Oct 16.
      Covalent inhibitors are an attractive targeting strategy that has expanded the development of degraders to target poorly druggable proteins including the E3 ligase RNF4. We show that RNF4 is a potential vulnerability of AML. High RNF4 expression levels correlate with poor patient survival and depletion of RNF4 results in increased sensitivity of AML cells to antileukemic drugs. Therefore, we aimed to develop chemical degraders (PROTACs) of RNF4 using a known covalent RNF4 ligand (CCW16), containing a chloro-N-acetamide group, as well as established E3 ligands targeting CRBN or VHL. However, while CCW16 and CCW16-derived PROTACs react potently with cysteines in recombinant RNF4, in cells, CCW16 forms covalent bonds with a large number of proteins, including peroxiredoxins. Consequently, CCW16 based PROTACs do not trigger degradation of RNF4, but induce the ferroptosis marker heme oxygenase-1 and impair cell viability in a distinct, RNF4-independent, ferroptotic cell death pathway. We hypothesize that other chloro-N-acetamide-containing E3 ligase ligands would also induce ferroptosis. Indeed, the RNF114 ligand EN219 also strongly induces ferroptosis, suggesting that ligands harboring this electrophile induce undesired off-target toxicity.
    Keywords:  AML; CCW16; Covalent PROTACs; Ferroptosis; RNF4
    DOI:  https://doi.org/10.1038/s44319-025-00593-4
  38. Methods Mol Biol. 2026 ;2976 25-34
      Fluorescent molecular probes have frequently been used to monitor lysosomal health, localization, abundance, and movement through the detection of acidic organelles and lysosomal enzyme activity. Flow cytometry technology provides rapid and accurate analysis of single cells (neurons) or particles (lysosomes) in suspension through laser detection. Herein, we describe how to detect lysosomes via LysoTracker™ and Magic Red® Cathepsin Activity assays in iPSC-derived human neuron cultures by flow cytometry.
    Keywords:  Flow cytometry; Fluorescent probes; Lysosome acidity; Lysosome function; iPSC-derived neuron cultures
    DOI:  https://doi.org/10.1007/978-1-0716-4844-5_3
  39. Anal Chim Acta. 2025 Dec 01. pii: S0003-2670(25)01007-4. [Epub ahead of print]1377 344613
      Mass Spectrometry Imaging (MSI) generates large datasets that require efficient computational solutions for data handling and visualization. While R and Python are commonly used for MSI analysis, their limited performance can hinder Big Data workflows. Julia is a high-performance programming language widely adopted in computationally demanding fields such as physics and economics. Here, we present JuliaMSI, a graphical user interface (GUI) developed in Julia for reading and analyzing MSI data in open formats (.imzML, .ibd, .mzML). JuliaMSI accelerates data loading, preprocessing, and visualization, with benchmarks showing up to 4.2-fold faster processing on Windows/macOS and 5.2-fold on Linux compared to R-based tools. Beyond speed, JuliaMSI enables interactive analysis through features such as contrast-enhancing filters (TrIQ, median filter), 3D topographic visualizations of ion intensity landscapes, and overlays of ion images with optical reference images. Users can inspect mass spectra linked to ion images, select regions of interest (ROI), and export results in publication-ready formats (.png, .jpg, .bmp). The platform supports seamless integration with downstream workflows via open data standards and provides a computationally efficient, user-friendly environment for large-scale MSI analysis. JuliaMSI is cross-platform (Linux, macOS, Windows) and available under the MIT license at https://codeberg.org/LabABI/JuliaMSI.
    Keywords:  Julia; Mass spectrometry imaging (MSI); Topography map; Visualization
    DOI:  https://doi.org/10.1016/j.aca.2025.344613
  40. Genome Biol. 2025 Oct 15. 26(1): 354
      Spatially resolved transcriptomics (SRT) facilitates the study of cell-cell interactions within native tissue environments. To support method development and benchmarking, we introduce sCCIgen, a real-data-based simulator that generates high-fidelity synthetic SRT data with known interaction features. sCCIgen preserves transcriptomic and spatial characteristics and provides key interaction features, including cell colocalization, spatial dependence of gene expression, and gene-gene interactions between neighboring cells. It supports input from SRT data, single-cell expression data alone, and unpaired expression and spatial data. sCCIgen is interactive, user-friendly, reproducible, and well-documented for studying cellular interactions and spatial biology.
    Keywords:  Cell–cell interaction; Data simulator; Spatially resolved transcriptomics
    DOI:  https://doi.org/10.1186/s13059-025-03762-9
  41. J Am Chem Soc. 2025 Oct 15.
      Cells are complex chemical systems capable of sensing and responding to environmental cues by dynamically reshaping themselves, e.g., by forming arm-like protrusions such as filopodia. Recapitulating cellular behavior in artificial systems is a long-standing goal in understanding the matter-to-life transition and designing responsive soft materials. Here, we use oil-in-water emulsions that mimic cellular environmental sensing and form directional arm-like filopodia in response to external chemical cues. Our work analyzes the step-by-step process involved in the formation of artificial filopodia, and we engineer ways to direct filopodia growth through different chemical gradients. The process is driven by asymmetric surfactant partitioning across the oil-water interface, followed by ordering at the interface to form lamellar structures, which are projected out as filopodia. We observe filopodia growing away from the source of kosmotropic anions and toward the source of chaotropic anions from the Hofmeister series. Significantly, these systems also respond to amino acid gradients, similar to cells: tryptophan gradients favor growth toward the source, while lysine and arginine gradients cause growth away from the amino acid source. Our findings open new avenues for fabricating life-like materials that sense and grow in response to external signals.
    DOI:  https://doi.org/10.1021/jacs.5c11719
  42. Cell Genom. 2025 Oct 16. pii: S2666-979X(25)00296-4. [Epub ahead of print] 101040
    Pancreatic Cancer Cohort Consortium
      Genetic and epigenetic variation in enhancers is associated with disease susceptibility; however, linking enhancers to target genes and predicting enhancer dysfunction remain challenging. We mapped enhancer-promoter interactions in human pancreas using 3D chromatin assays across 28 donors and five cell types. Using a network approach, we parsed these interactions into enhancer-promoter tree models, enabling quantitative, genome-wide analysis of enhancer connectivity. A machine learning algorithm built on these trees estimated enhancer contributions to cell-type-specific gene expression. To test predictions, we perturbed enhancers in primary human pancreas cells with CRISPR interference and quantified effects at single-cell resolution using RNA fluorescence in situ hybridization (FISH) and high-throughput imaging. Tree models also annotated germline risk variants linked to pancreatic disorders, connecting them to candidate target genes. For pancreatic ductal adenocarcinoma risk, acinar regulatory elements showed greater variant enrichment, challenging the ductal cell-of-origin view. Together, these datasets and models provide a resource for studying pancreatic disease genetics.
    Keywords:  3D genome organization; CRISPR; GWAS; cell identity; diabetes; enhancer; graph models; noncoding variants; pancreas; pancreatic cancer
    DOI:  https://doi.org/10.1016/j.xgen.2025.101040