bims-cagime Biomed News
on Cancer, aging and metabolism
Issue of 2024‒09‒15
25 papers selected by
Kıvanç Görgülü, Technical University of Munich



  1. Biochem J. 2024 Sep 18. 481(18): 1187-1202
      Phosphatidylinositol is a precursor of various phosphoinositides, which play crucial roles in intracellular signaling and membrane dynamics and have impact on diverse aspects of cell physiology. Phosphoinositide synthesis and turnover occur in the cytoplasmic leaflet of the organellar and plasma membranes. P4-ATPases (lipid flippases) are responsible for translocating membrane lipids from the exoplasmic (luminal) to the cytoplasmic leaflet, thereby regulating membrane asymmetry. However, the mechanism underlying phosphatidylinositol translocation across cellular membranes remains elusive. Here, we discovered that the phosphatidylcholine flippases ATP8B1, ATP8B2, and ATP10A can also translocate phosphatidylinositol at the plasma membrane. To explore the function of these phosphatidylinositol flippases, we used cells depleted of CDC50A, a protein necessary for P4-ATPase function and ATP8B1 and ATP8B2, which express in HeLa cells. Upon activation of the Gq-coupled receptor, depletion of phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] was accelerated in CDC50A knockout (KO) and ATP8B1/8B2 double KO cells compared with control cells, suggesting a decrease in PtdIns(4,5)P2 levels within the plasma membrane of the KO cells upon stimulation. These findings highlight the important role of P4-ATPases in maintaining phosphoinositide homeostasis and suggest a mechanism for asymmetry of phosphatidylinositol in the cytoplasmic leaflet of the plasma membrane.
    Keywords:  P4-ATPase; flippase; lipid transport; phosphatidylinositol; phosphoinositide
    DOI:  https://doi.org/10.1042/BCJ20240223
  2. Nat Metab. 2024 Sep 09.
      While heterogeneity is a key feature of cancer, understanding metabolic heterogeneity at the single-cell level remains a challenge. Here we present 13C-SpaceM, a method for spatial single-cell isotope tracing that extends the previously published SpaceM method with detection of 13C6-glucose-derived carbons in esterified fatty acids. We validated 13C-SpaceM on spatially heterogeneous models using liver cancer cells subjected to either normoxia-hypoxia or ATP citrate lyase depletion. This revealed substantial single-cell heterogeneity in labelling of the lipogenic acetyl-CoA pool and in relative fatty acid uptake versus synthesis hidden in bulk analyses. Analysing tumour-bearing brain tissue from mice fed a 13C6-glucose-containing diet, we found higher glucose-dependent synthesis of saturated fatty acids and increased elongation of essential fatty acids in tumours compared with healthy brains. Furthermore, our analysis uncovered spatial heterogeneity in lipogenic acetyl-CoA pool labelling in tumours. Our method enhances spatial probing of metabolic activities in single cells and tissues, providing insights into fatty acid metabolism in homoeostasis and disease.
    DOI:  https://doi.org/10.1038/s42255-024-01118-4
  3. bioRxiv. 2024 Aug 27. pii: 2024.08.26.609758. [Epub ahead of print]
      Both membranes and biopolymers can individually separate into coexisting liquid phases. Here we explore biopolymer prewetting at membranes, a phase transition that emerges when these two thermodynamic systems are coupled. In reconstitution, we couple short poly-L-Lysine and poly-L-Glutamic Acid polyelectrolytes to membranes of saturated lipids, unsaturated lipids, and cholesterol, and detect coexisting prewet and dry surface phases well outside of the region of coexistence for each individual system. Notability, polyelectrolyte prewetting is highly sensitive to membrane lipid composition, occurring at 10 fold lower polymer concentration in a membrane close to its phase transition compared to one without a phase transition. In cells, protein prewetting is achieved using an optogenetic tool that enables titration of condensing proteins and tethering to the plasma membrane inner leaflet. Here we show that protein prewetting occurs for conditions well outside those where proteins condense in the cytoplasm, and that the stability of prewet domains is sensitive to perturbations of plasma membrane composition and structure. Our work presents an example of how thermodynamic phase transitions can impact cellular structure outside their individual coexistence regions, suggesting new possible roles for phase-separation-prone systems in cell biology.
    DOI:  https://doi.org/10.1101/2024.08.26.609758
  4. J Cell Sci. 2024 Sep 11. pii: jcs.262166. [Epub ahead of print]
      Environment-sensitive probes are frequently used in spectral/multi-channel microscopy to study alterations in cell homeostasis. However, the few open-source packages available for processing of spectral images are limited in scope. Here, we present VISION, a stand-alone software based on Python for spectral analysis with improved applicability. In addition to classical intensity-based analysis, our software can batch-process multidimensional images with an advanced single-cell segmentation capability and apply user-defined mathematical operations on spectra to calculate biophysical and metabolic parameters of single cells. VISION allows for 3D and temporal mapping of properties such as membrane fluidity and mitochondrial potential. We demonstrate the broad applicability of VISION by applying it to study the effect of various drugs on cellular biophysical properties; the correlation between membrane fluidity and mitochondrial potential; protein distribution in cell-cell contacts; and properties of nanodomains in cell-derived vesicles. Together with the code, we provide a graphical user interface for facile adoption.
    Keywords:  Biophysical Properties; Image analysis; Multi-dimension microscopy; Open source; Python; Spectral Imaging
    DOI:  https://doi.org/10.1242/jcs.262166
  5. Proc Natl Acad Sci U S A. 2024 Sep 17. 121(38): e2401241121
      Despite longstanding excitement and progress toward understanding liquid-liquid phase separation in natural and artificial membranes, fundamental questions have persisted about which molecules are required for this phenomenon. Except in extraordinary circumstances, the smallest number of components that has produced large-scale, liquid-liquid phase separation in bilayers has stubbornly remained at three: a sterol, a phospholipid with ordered chains, and a phospholipid with disordered chains. This requirement of three components is puzzling because only two components are required for liquid-liquid phase separation in lipid monolayers, which resemble half of a bilayer. Inspired by reports that sterols interact closely with lipids with ordered chains, we tested whether phase separation would occur in bilayers in which a sterol and lipid were replaced by a single, joined sterol-lipid. By evaluating a panel of sterol-lipids, some of which are present in bacteria, we found a minimal bilayer of only two components (PChemsPC and diPhyPC) that robustly demixes into micron-scale, liquid phases. It suggests an additional role for sterol-lipids in nature, and it reveals a membrane in which tie-lines (and, therefore, the lipid composition of each phase) are straightforward to determine and will be consistent across multiple laboratories.
    Keywords:  lipid; liquid–liquid phase separation; membrane; sterol
    DOI:  https://doi.org/10.1073/pnas.2401241121
  6. Cancer Cell. 2024 Sep 12. pii: S1535-6108(24)00314-3. [Epub ahead of print]
      Brain metastasis, a serious complication of cancer, hinges on the initial survival, microenvironment adaptation, and outgrowth of disseminated cancer cells. To understand the early stages of brain colonization, we investigated two prevalent sources of cerebral relapse, triple-negative (TNBC) and HER2+ (HER2BC) breast cancers. Using mouse models and human tissue samples, we found that these tumor types colonize the brain, with a preference for distinctive tumor architectures, stromal interfaces, and autocrine programs. TNBC models tend to form perivascular sheaths with diffusive contact with astrocytes and microglia. In contrast, HER2BC models tend to form compact spheroids driven by autonomous tenascin C production, segregating stromal cells to the periphery. Single-cell transcriptomics of the tumor microenvironment revealed that these architectures evoke differential Alzheimer's disease-associated microglia (DAM) responses and engagement of the GAS6 receptor AXL. The spatial features of the two modes of brain colonization have relevance for leveraging the stroma to treat brain metastasis.
    Keywords:  brain metastasis; breast cancer; extracellular matrix; microglia; tumor architecture; tumor microenvironment
    DOI:  https://doi.org/10.1016/j.ccell.2024.08.015
  7. Mol Oncol. 2024 Sep 10.
      Pancreatic ductal adenocarcinoma (PDAC) has limited treatment options, emphasizing the urgent need for effective therapies. The predominant driver in PDAC is mutated KRAS proto-oncogene, KRA, present in 90% of patients. The emergence of direct KRAS inhibitors presents a promising avenue for treatment, particularly those targeting the KRASG12C mutated allele, which show encouraging results in clinical trials. However, the development of resistance necessitates exploring potent combination therapies. Our objective was to identify effective KRASG12C-inhibitor combination therapies through unbiased drug screening. Results revealed synergistic effects with son of sevenless homolog 1 (SOS1) inhibitors, tyrosine-protein phosphatase non-receptor type 11 (PTPN11)/Src homology region 2 domain-containing phosphatase-2 (SHP2) inhibitors, and broad-spectrum multi-kinase inhibitors. Validation in a novel and unique KRASG12C-mutated patient-derived organoid model confirmed the described hits from the screening experiment. Our findings propose strategies to enhance KRASG12C-inhibitor efficacy, guiding clinical trial design and molecular tumor boards.
    Keywords:  KRASG12C; SHP2; SOS1; pancreatic cancer
    DOI:  https://doi.org/10.1002/1878-0261.13725
  8. Cancer Metab. 2024 Sep 06. 12(1): 26
      BACKGROUND: PAF1/PD2 deregulation contributes to tumorigenesis, drug resistance, and cancer stem cell maintenance in Pancreatic Cancer (PC). Recent studies demonstrate that metabolic reprogramming plays a role in PC progression, but the mechanism is poorly understood. Here, we focused on examining the role of PAF1/PD2 in the metabolic rewiring of PC.METHODS: Cell lines were transfected with shRNAs to knockdown PAF1/PD2. Metabolic genes regulated by PAF1/PD2 were identified by qPCR/western blot, and metabolic assays were performed. Immunoprecipitations/ChIP were performed to identify PAF1/PD2 protein partners and confirm PAF1/HIF1α sub-complex binding to LDHA.
    RESULTS: PAF1 and LDHA showed progressively increased expression in human pancreatic tumor sections. Aerobic glycolysis genes were downregulated in PAF1-depleted PC cells. Metabolic assays indicated a decreased lactate production and glucose uptake in knockdown cells. Furthermore, PAF1/PD2 depletion showed a reduced glycolytic rate and increased oxidative phosphorylation by ECAR and OCR analysis. Interestingly, we identified that HIF1α interacts and co-localizes with PAF1, specifically in PC cells. We also observed that the PAF1/PD2-HIF1α complex binds to the LDHA promoter to regulate its expression, reprogramming the metabolism to utilize the aerobic glycolysis pathway preferentially.
    CONCLUSION: Overall, the results indicate that PAF1/PD2 rewires PC metabolism by interacting with HIF1α to regulate the expression of LDHA.
    Keywords:  Aerobic glycolysis; Metabolism; Pancreatic cancer
    DOI:  https://doi.org/10.1186/s40170-024-00354-2
  9. Nat Rev Drug Discov. 2024 Sep 06.
      As the field of cancer neuroscience expands, the strategic targeting of interactions between neurons, cancer cells and other elements in the tumour microenvironment represents a potential paradigm shift in cancer treatment, comparable to the advent of our current understanding of tumour immunology. Cancer cells actively release growth factors that stimulate tumour neo-neurogenesis, and accumulating evidence indicates that tumour neo-innervation propels tumour progression, inhibits tumour-related pro-inflammatory cytokines, promotes neovascularization, facilitates metastasis and regulates immune exhaustion and evasion. In this Review, we give an up-to-date overview of the dynamics of the tumour microenvironment with an emphasis on tumour innervation by the peripheral nervous system, as well as current preclinical and clinical evidence of the benefits of targeting the nervous system in cancer, laying a scientific foundation for further clinical trials. Combining empirical data with a biomarker-driven approach to identify and hone neuronal targets implicated in cancer and its spread can pave the way for swift clinical integration.
    DOI:  https://doi.org/10.1038/s41573-024-01017-z
  10. Cell. 2024 Aug 29. pii: S0092-8674(24)00905-X. [Epub ahead of print]
      Epithelial-to-mesenchymal transitions (EMTs) and extracellular matrix (ECM) remodeling are distinct yet important processes during carcinoma invasion and metastasis. Transforming growth factor β (TGF-β) and RAS, signaling through SMAD and RAS-responsive element-binding protein 1 (RREB1), jointly trigger expression of EMT and fibrogenic factors as two discrete arms of a common transcriptional response in carcinoma cells. Here, we demonstrate that both arms come together to form a program for lung adenocarcinoma metastasis and identify chromatin determinants tying the expression of the constituent genes to TGF-β and RAS inputs. RREB1 localizes to H4K16acK20ac marks in histone H2A.Z-loaded nucleosomes at enhancers in the fibrogenic genes interleukin-11 (IL11), platelet-derived growth factor-B (PDGFB), and hyaluronan synthase 2 (HAS2), as well as the EMT transcription factor SNAI1, priming these enhancers for activation by a SMAD4-INO80 nucleosome remodeling complex in response to TGF-β. These regulatory properties segregate the fibrogenic EMT program from RAS-independent TGF-β gene responses and illuminate the operation and vulnerabilities of a bifunctional program that promotes metastatic outgrowth.
    Keywords:  EMT; RAS; SMAD; TGF-β; chromatin; enhancer; fibrosis; lung adenocarcinoma; metastasis
    DOI:  https://doi.org/10.1016/j.cell.2024.08.014
  11. Nat Commun. 2024 Sep 12. 15(1): 7662
      Most patients with advanced cancer develop cachexia, a multifactorial syndrome characterized by progressive skeletal muscle wasting. Despite its catastrophic impact on survival, the critical mediators responsible for cancer cachexia development remain poorly defined. Here, we show that a distinct subset of neutrophil-like monocytes, which we term cachexia-inducible monocytes (CiMs), emerges in the advanced cancer milieu and promotes skeletal muscle loss. Unbiased transcriptome analysis reveals that interleukin 36 gamma (IL36G)-producing CD38+ CiMs are induced in chronic monocytic blood cancer characterized by prominent cachexia. Notably, the emergence of CiMs and the activation of CiM-related gene signatures in monocytes are confirmed in various advanced solid cancers. Stimuli of toll-like receptor 4 signaling are responsible for the induction of CiMs. Genetic inhibition of IL36G-mediated signaling attenuates skeletal muscle loss and rescues cachexia phenotypes in advanced cancer models. These findings indicate that the IL36G-producing subset of neutrophil-like monocytes could be a potential therapeutic target in cancer cachexia.
    DOI:  https://doi.org/10.1038/s41467-024-51873-x
  12. bioRxiv. 2024 Sep 04. pii: 2024.08.28.610209. [Epub ahead of print]
      Caveolin is a monotopic integral membrane protein, widely expressed in metazoa and responsible for constructing enigmatic membrane invaginations known as caveolae. Recently, the high-resolution structure of a purified human caveolin assembly, the CAV1-8S complex, revealed a unique organization of 11 protomers arranged in a tightly packed, radially symmetric spiral disc. One face and the outer rim of this disc are highly hydrophobic, suggesting that the complex incorporates into membranes by displacing hundreds of lipids from one leaflet. The feasibility of this unique molecular architecture and its biophysical and functional consequences are currently unknown. Using Langmuir film balance measurements, we find that CAV1-8S is highly surface active and intercalates into lipid monolayers. Molecular simulations of biomimetic bilayers support this 'leaflet replacement' model and reveal that while CAV1-8S effectively displaces phospholipids from one bilayer leaflet, it accumulates 40-70 cholesterol molecules into a disordered monolayer between the complex and its distal lipid leaflet. We find that CAV1-8S preferentially associates with positively curved membrane surfaces due to its influence on the conformations of distal leaflet lipids, and that these effects laterally sort lipids of the distal leaflet. Large-scale simulations of multiple caveolin assemblies confirmed their association with large, positively curved membrane morphologies, consistent with the shape of caveolae. Further, association with curved membranes regulates the exposure of caveolin residues implicated in protein-protein interactions. Altogether, the unique structure of CAV1-8S imparts unusual modes of membrane interaction with implications for membrane organization, morphology, and physiology.STATEMENT OF SIGNIFICANCE: Caveolae are membrane invaginations heavily implicated in cellular physiology and disease; however, how their unique shape and function are produced remains enigmatic. Here, following on recent characterization of the unusual structure of the CAV1-8S oligomer, we examine the molecular details of its interactions with its solvating lipid membrane. We describe a novel mode of membrane interaction-which we term 'leaflet replacement'-for the CAV1-8S complex that has not previously been observed for any other protein. The biophysical consequences of this unique molecular organization provide mechanistic insights into the functions and organization of caveolae in cells.
    DOI:  https://doi.org/10.1101/2024.08.28.610209
  13. Nat Rev Cancer. 2024 Sep 09.
      Solid tumours comprise cancer cells that engage in continuous interactions with non-malignant cells and with acellular components, forming the tumour microenvironment (TME). The TME has crucial and diverse roles in tumour progression and metastasis, and substantial efforts have been dedicated into understanding the functions of different cell types within the TME. These efforts highlighted the importance of non-cell-autonomous signalling in cancer, mediating interactions between the cancer cells, the immune microenvironment and the non-immune stroma. Much of this non-cell-autonomous signalling is mediated through acellular components of the TME, known as the extracellular matrix (ECM), and controlled by the cells that secrete and remodel the ECM - the cancer-associated fibroblasts (CAFs). In this Review, we delve into the complex crosstalk among cancer cells, CAFs and immune cells, highlighting the effects of CAF-induced ECM remodelling on T cell functions and offering insights into the potential of targeting ECM components to improve cancer therapies.
    DOI:  https://doi.org/10.1038/s41568-024-00740-4
  14. Cancer Discov. 2024 Sep 09.
      Aneuploidy results in a stoichiometric imbalance of protein complexes that jeopardizes cellular fitness. Aneuploid cells thus need to compensate for the imbalanced DNA levels by regulating their RNA and protein levels, but the underlying molecular mechanisms remain unknown. Here, we dissected multiple diploid vs. aneuploid cell models. We found that aneuploid cells cope with transcriptional burden by increasing several RNA degradation pathways, and are consequently more sensitive to the perturbation of RNA degradation. At the protein level, aneuploid cells mitigate proteotoxic stress by reducing protein translation and increasing protein degradation, rendering them more sensitive to proteasome inhibition. These findings were recapitulated across hundreds of human cancer cell lines and primary tumors, and aneuploidy levels were significantly associated with the response of multiple myeloma patients to proteasome inhibitors. Aneuploid cells are therefore preferentially dependent on several key nodes along the gene expression process, creating clinically-actionable vulnerabilities in aneuploid cells.
    DOI:  https://doi.org/10.1158/2159-8290.CD-23-0309
  15. Autophagy. 2024 Sep 12.
      DBI/ACBP (diazepam binding inhibitor, acyl-CoA binding protein) is produced by multiple cell types and detectable in blood plasma. DBI acts on GABRA (gamma-aminobutyric acid type A receptor) complexes containing GABRG2 (gamma-aminobutyric acid type A receptor, subunit gamma 2) to inhibit macroautophagy/autophagy and hence can be considered as an "autophagy checkpoint". In patients with poor-prognosis anorexia nervosa, as well as in mice developing stress-induced anorexia, circulating DBI levels are reduced. Using a chemical-genetic system that makes it possible to control DBI secretion by hepatocytes, we showed that increasing DBI levels suffice to prevent anorexia induced by chronic restraint stress or chemotherapy with cisplatin, doxorubicin or paclitaxel in mice. At the mechanistic level, DBI administration acts through GABRA outside of the central nervous system and reduces the plasma levels of anorexigenic factors such as GDF15 (growth differentiation factor 15) and LCN2 (lipocalin 2), as well as anorexigenic signaling via the LCN2 receptor MC4R (melanocortin 4 receptor) in the hypothalamus. Accordingly, DBI supplementation stimulates food intake and normalizes whole body weight, body composition and metabolism in mouse models of anorexia. This normalization extends to the liver transcriptome and metabolome. Altogether, it appears that enhancing DBI levels constitutes a promising strategy for combating anorexia.
    Keywords:  Appetite control; autophagy; body mass index; endozepine; metabolism; obesity
    DOI:  https://doi.org/10.1080/15548627.2024.2402162
  16. iScience. 2024 Sep 20. 27(9): 110642
      Etomoxir has been used for decades as a popular small molecule inhibitor of carnitine palmitoyltransferase I, Cpt1, to block mitochondrial fatty acid β-oxidation. To test the specificity of etomoxir, we generated click chemistry-enabled reagents to label etomoxir binding proteins in situ. Etomoxir bound to Cpt1, but also bound to a large array of diverse proteins that metabolize and transport fatty acids in the cytoplasm, peroxisome, and mitochondria. Many of the most abundant proteins identified in primary hepatocytes were peroxisomal proteins. The loss of Pex5, required for the import of peroxisomal matrix proteins, eliminated many of these etomoxir-labeled proteins. By utilizing the promiscuous, covalent, and fatty acid mimetic properties of etomoxir, etomoxir targets of fatty acid ω-oxidation were revealed following the loss of Pex5. These data demonstrate that etomoxir is not specific for Cpt1 and is not appropriate as a tool to distinguish the biological effects of fatty acid oxidation.
    Keywords:  Biochemistry; Chemical compound; Enzymology; Molecular biology; Molecular interaction
    DOI:  https://doi.org/10.1016/j.isci.2024.110642
  17. Cell. 2024 Sep 05. pii: S0092-8674(24)00896-1. [Epub ahead of print]187(18): 4830-4832
      Building biological computers is one of the most intensively pursued goals of modern synthetic biology. The new TriLoS tristate-based logic synthesis platform, published in this issue of Cell, offers a long-awaited solution to scale up the complexity of biocomputing, opening a path to move this field beyond proof-of-principle demonstrations.
    DOI:  https://doi.org/10.1016/j.cell.2024.08.005
  18. Pigment Cell Melanoma Res. 2024 Sep 10.
      As efforts to study the mechanisms of melanoma metastasis and novel therapeutic approaches multiply, researchers need accurate, high-throughput methods to evaluate the effects on tumor burden resulting from specific interventions. We show that automated quantification of tumor content from whole slide images is a compelling solution to assess in vivo experiments. In order to increase the outflow of data collection from preclinical studies, we assembled a large dataset with annotations and trained a deep neural network for the quantitative analysis of melanoma tumor content on histopathological sections of murine models. After assessing its performance in segmenting these images, the tool obtained consistent results with an orthogonal method (bioluminescence) of measuring metastasis in an experimental setting. This AI-based algorithm, made freely available to academic laboratories through a web-interface called MetFinder, promises to become an asset for melanoma researchers and pathologists interested in accurate, quantitative assessment of metastasis burden.
    Keywords:  deep learning; histopathology; metastatic burden; murine models; preclinical studies; quantification; whole slide images
    DOI:  https://doi.org/10.1111/pcmr.13195
  19. bioRxiv. 2024 Aug 26. pii: 2024.08.26.609529. [Epub ahead of print]
      Collective migration of epithelial tissues is a critical feature of developmental morphogenesis and tissue homeostasis. Coherent motion of cell collectives requires large scale coordination of motion and force generation and is influenced by mechanical properties of the underlying substrate. While tissue viscoelasticity is a ubiquitous feature of biological tissues, its role in mediating collective cell migration is unclear. Here, we have investigated the impact of substrate stress relaxation on the migration of micropatterned epithelial monolayers. Epithelial monolayers exhibit faster collective migration on viscoelastic alginate substrates with slower relaxation timescales, which are more elastic, relative to substrates with faster stress relaxation, which exhibit more viscous loss. Faster migration on slow-relaxing substrates is associated with reduced substrate deformation, greater monolayer fluidity, and enhanced leader cell formation. In contrast, monolayers on fast-relaxing substrates generate substantial substrate deformations and are more jammed within the bulk, with reduced formation of transient lamellipodial protrusions past the monolayer edge leading to slower overall expansion. This work reveals features of collective epithelial dynamics on soft, viscoelastic materials and adds to our understanding of cell-substrate interactions at the tissue scale.Significance Statement: Groups of cells must coordinate their movements in order to sculpt organs during development and maintain tissues. The mechanical properties of the underlying substrate on which cells reside are known to influence key aspects of single and collective cell migration. Despite being a nearly universal feature of biological tissues, the role of viscoelasticity (i.e., fluid-like and solid-like behavior) in collective cell migration is unclear. Using tunable engineered biomaterials, we demonstrate that sheets of epithelial cells display enhanced migration on slower-relaxing (more elastic) substrates relative to faster-relaxing (more viscous) substrates. Building our understanding of tissue-substrate interactions and collective cell dynamics provides insights into approaches for tissue engineering and regenerative medicine, and therapeutic interventions to promote health and treat disease.
    DOI:  https://doi.org/10.1101/2024.08.26.609529
  20. Autophagy. 2024 Sep 08.
      Macroautophagy/autophagy is a constitutively active catabolic lysosomal degradation pathway, often found dysregulated in human diseases. It is often considered to act in a cytoprotective manner and is commonly upregulated in cells undergoing stress. Its initiation is regulated at the protein level and does not require de novo protein synthesis. Historically, autophagy has been regarded as non-selective; however, it is now clear that different stimuli can lead to the selective degradation of cellular components via selective autophagy receptors (SARs). Due to its selective nature and the existence of multiple degradation pathways potentially acting in concert, monitoring of autophagy flux, i.e. selective autophagy-dependent protein degradation, should address this complexity. Here, we introduce a targeted proteomics approach monitoring abundance changes of 37 autophagy-related proteins covering process-relevant proteins such as the initiation complex and the Atg8-family protein lipidation machinery, as well as most known SARs. We show that proteins involved in autophagosome biogenesis are upregulated and spared from degradation under autophagy-inducing conditions in contrast to SARs, in a cell-line dependent manner. Classical bulk stimuli such as nutrient starvation mainly induce degradation of ubiquitin-dependent soluble SARs and not of ubiquitin-independent, membrane-bound SARs. In contrast, treatment with the iron chelator deferiprone leads to the degradation of ubiquitin-dependent and -independent SARs linked to mitophagy and reticulophagy/ER-phagy. Our approach is automatable and supports large-scale screening assays paving the way to (pre)clinical applications and monitoring of specific autophagy flux.
    Keywords:  ER-phagy; mass spectrometry; mitophagy; parallel reaction monitoring; reticulophagy; selective autophagy receptors
    DOI:  https://doi.org/10.1080/15548627.2024.2396792
  21. Nat Methods. 2024 Sep 10.
      Single-molecule localization microscopy (SMLM) has gained widespread use for visualizing the morphology of subcellular organelles and structures with nanoscale spatial resolution. However, analysis tools for automatically quantifying and classifying SMLM images have lagged behind. Here we introduce Enhanced Classification of Localized Point clouds by Shape Extraction (ECLiPSE), an automated machine learning analysis pipeline specifically designed to classify cellular structures captured through two-dimensional or three-dimensional SMLM. ECLiPSE leverages a comprehensive set of shape descriptors, the majority of which are directly extracted from the localizations to minimize bias during the characterization of individual structures. ECLiPSE has been validated using both unsupervised and supervised classification on datasets, including various cellular structures, achieving near-perfect accuracy. We apply two-dimensional ECLiPSE to classify morphologically distinct protein aggregates relevant for neurodegenerative diseases. Additionally, we employ three-dimensional ECLiPSE to identify relevant biological differences between healthy and depolarized mitochondria. ECLiPSE will enhance the way we study cellular structures across various biological contexts.
    DOI:  https://doi.org/10.1038/s41592-024-02414-3
  22. Nat Cell Biol. 2024 Sep 11.
      Ammonia is thought to be a cytotoxin and its increase in the blood impairs cell function. However, whether and how this toxin triggers cell death under pathophysiological conditions remains unclear. Here we show that ammonia induces a distinct form of cell death in effector T cells. We found that rapidly proliferating T cells use glutaminolysis to release ammonia in the mitochondria, which is then translocated to and stored in the lysosomes. Excessive ammonia accumulation increases lysosomal pH and results in the termination of lysosomal ammonia storage and ammonia reflux into mitochondria, leading to mitochondrial damage and cell death, which is characterized by lysosomal alkalization, mitochondrial swelling and impaired autophagic flux. Inhibition of glutaminolysis or blocking lysosomal alkalization prevents ammonia-induced T cell death and improves T cell-based antitumour immunotherapy. These findings identify a distinct form of cell death that differs from previously known mechanisms.
    DOI:  https://doi.org/10.1038/s41556-024-01503-x
  23. J Cell Physiol. 2024 Sep 08. e31417
      Neoplastic transformation reprograms tumor and surrounding host cell metabolism, increasing nutrient consumption and depletion in the tumor microenvironment. Tumors uptake nutrients from neighboring normal tissues or the bloodstream to meet energy and anabolic demands. Tumor-induced chronic inflammation, a high-energy process, also consumes nutrients to sustain its dysfunctional activities. These tumor-related metabolic and physiological changes, including chronic inflammation, negatively impact systemic metabolism and physiology. Furthermore, the adverse effects of antitumor therapy and tumor obstruction impair the endocrine, neural, and gastrointestinal systems, thereby confounding the systemic status of patients. These alterations result in decreased appetite, impaired nutrient absorption, inflammation, and shift from anabolic to catabolic metabolism. Consequently, cancer patients often suffer from malnutrition, which worsens prognosis and increases susceptibility to secondary adverse events. This review explores how neoplastic transformation affects tumor and microenvironment metabolism and inflammation, leading to poor prognosis, and discusses potential strategies and clinical interventions to improve patient outcomes.
    Keywords:  cachexia; cancer metabolism; detary interventions; inflammation; malnutrition
    DOI:  https://doi.org/10.1002/jcp.31417