bims-cesirm Biomed News
on Cell Signaling mediated regulation of metabolism
Issue of 2025–09–14
eleven papers selected by
Tigist Tamir, University of North Carolina



  1. Nat Metab. 2025 Sep 09.
      The essential cofactor coenzyme A (CoASH) and its thioester derivatives (acyl-CoAs) have pivotal roles in cellular metabolism. However, the mechanism by which different acyl-CoAs are accurately partitioned into different subcellular compartments to support site-specific reactions, and the physiological impact of such compartmentalization, remain poorly understood. Here, we report an optimized liquid chromatography-mass spectrometry-based pan-chain acyl-CoA extraction and profiling method that enables a robust detection of 33 cellular and 23 mitochondrial acyl-CoAs from cultured human cells. We reveal that SLC25A16 and SLC25A42 are critical for mitochondrial import of free CoASH. This CoASH import process supports an enriched mitochondrial CoA pool and CoA-dependent pathways in the matrix, including the high-flux TCA cycle and fatty acid oxidation. Despite a small fraction of the mitochondria-localized CoA synthase COASY, de novo CoA biosynthesis is primarily cytosolic and supports cytosolic lipid anabolism. This mitochondrial acyl-CoA compartmentalization enables a spatial regulation of anabolic and energy-related catabolic processes, which promises to shed light on pathophysiology in the inborn errors of CoA metabolism.
    DOI:  https://doi.org/10.1038/s42255-025-01358-y
  2. J Endocr Soc. 2025 Oct;9(10): bvaf131
      Although indicated as adjunctive therapy for seizure disorders, ketogenic diets (KDs) have gained popularity for weight loss and mitigating the metabolic risks associated with severe obesity. However, efficacy, durability, and long-term consequences are incompletely understood. In preclinical models, most studies have included only male mice, precluding an understanding of sex-specific responses to KD. In this study, we investigated sex differences in response to a high-fat, low carbohydrate, low-protein KD using male and female C57BL/6J mice. Despite equivalent circulating levels of β-hydroxybutyrate, male mice exhibited weight loss characterized by loss of fat mass and lean mass in concert with increased energy expenditure. In contrast, female mice exhibited increased fat mass and body weight on the KD. Male mice manifested increased insulin sensitivity, without reducing glucose excursions during glucose tolerance testing, in concert with decreased glucose-stimulated insulin release. In contrast, females developed glucose intolerance and insulin resistance relative to control females. Following oophorectomy, female mice lost weight on KD but remained glucose intolerant. Orchidectomy in male mice reversed weight loss in KD males. Circulating fibroblast growth factor 21 (FGF21) concentrations were increased in males but not females on KD and correlated with increased FGF21 expression in brown adipose tissue. These findings demonstrate that the metabolic effects of KD are sex-specific and suggest that gonadal hormones modulate the adaptive response to ketogenic diets via FGF21 signaling.
    Keywords:  FGF21; gonadal hormones; insulin resistance; ketogenic diet; sex differences
    DOI:  https://doi.org/10.1210/jendso/bvaf131
  3. Cancers (Basel). 2025 Sep 02. pii: 2882. [Epub ahead of print]17(17):
      Background/Objectives: HER2, a critical diagnostic marker and therapeutic target in breast cancer, is a membrane receptor that forms diverse signaling complexes, the constituents of which have not been fully characterized in actual breast cancer tissues. Methods: In this study, we applied the Rapid Immunoprecipitation Mass Spectrometry of Endogenous Proteins (RIME) method, originally developed to explore transcription factor complexes, to identify the complexes formed by HER2 in HER2-positive breast cancer specimens. Results: Through our approach, we successfully identified multiple complex components, including MARCKS, a novel HER2-interacting partner, which we verified using both proximal ligation assay in cultured cells and immunohistochemistry in tissue sections. TCGA analysis further revealed that high MARCKS expression significantly correlates with ER negativity, as confirmed by multivariate analysis, suggesting its potential role as a prognostic indicator in aggressive breast cancer subtypes. Conclusions: These results demonstrate the capability of RIME to elucidate interactomes of membrane proteins such as HER2 in clinical tissue specimens. Furthermore, this study highlights its broader applicability beyond nuclear proteins, underscoring its potential for discovering novel prognostic and diagnostic clinical markers in diverse cancer types.
    Keywords:  HER2; MARCKS; Mass Spectrometry; RIME; TCGA; biomarker; breast cancer; interactome; proteomics
    DOI:  https://doi.org/10.3390/cancers17172882
  4. Sci Adv. 2025 Sep 12. 11(37): eadx4511
      Posttranslational protein modifications have emerged as a mechanism regulating progenitor cell state transitions during tissue formation. Herein, we exploit the stereotyped hair follicle development to delineate the function of PADI4, an enzyme converting peptidylarginine to citrulline. Single-cell sequencing places Padi4 in both progenitor and differentiated hair lineage cells and indicates that PADI4 acts to repress transcription during hair follicle development. We establish PADI4 as a negative regulator of proliferation, acting on LEF1-positive hair shaft committed progenitor cells. Mechanistically, PADI4 citrullinates proteins associated with mRNA processing and ribosomal biogenesis, and lack of PADI4 promotes protein synthesis and ribosomal RNA transcription in vivo. Characterizing key translational effectors, we demonstrate that PADI4 citrullinates the translational repressor 4E-BP1 and reveal a cross-talk between PADI4 activity and 4E-BP1 phosphorylation. This work sheds light on how posttranslational modifications affect progenitor cell states and tissue formation.
    DOI:  https://doi.org/10.1126/sciadv.adx4511
  5. mSystems. 2025 Sep 08. e0056925
      Histoplasma capsulatum is a human fungal pathogen that survives and proliferates within phagocytic immune cells. To sustain growth in the nutrient-limited phagosome environment, the pathogenic yeast scavenges available carbon sources, which must be metabolized through central carbon metabolism for respiration and biomass synthesis. However, Histoplasma carbon metabolic pathways operating in the pathogenic yeast phase have not been extensively mapped. To address this gap, we employed a fluxomic platform using stable isotope tracers to quantify the cellular reaction rates of central carbon metabolism. This approach revealed that, in Histoplasma yeasts, carbon resides within five main reservoirs: fatty acids, proteins, mannitol, nucleic acids, and cell wall components. Carbon conversion efficiency, or biomass yield, was approximately 50%, indicating substantial CO2 loss from supplemented carbon substrates, glucose, and glutamate. 13C-labeling analysis demonstrated simultaneous glycolysis and gluconeogenesis, and enriched serine labeling confirmed threonine aldolase activity in serine biosynthesis. Compartmentalization of pyruvate metabolism was evident from the labeling of amino acids derived from pyruvate, with the methylcitrate cycle identified as the primary source of labeled pyruvate. Notably, malic enzyme and pyruvate carboxylase exhibited negligible fluxes, while mitochondrial reactions, particularly CO2-producing ones, were the most active. These results offer insight into key metabolic reactions, alternative pathways, and metabolite/enzyme compartmentalization in Histoplasma yeast metabolism. This foundational framework supports future studies aimed at identifying metabolic targets for novel histoplasmosis therapeutics.IMPORTANCETo our knowledge, this study represents the first application of 13C-metabolic flux analysis to a human fungal pathogen, where we identified carbon reservoirs and quantified the metabolic fluxes of pathogenic Histoplasma yeasts. Our findings demonstrated that Histoplasma metabolizes carbon toward cellular respiration to robustly produce CO2 and energy but also uses alternative pathways within central metabolism for biosynthesis. Given the potential for other pathogenic fungi to share similar metabolic features, especially biomass, our study offers a comprehensive framework for deciphering fungal metabolism, providing insights into their infection-enabling metabolism and offering a foundation for identifying new therapeutic targets.
    Keywords:  Histoplasmosis; Metabolic flux analysis; biomass; carbon flux map; fungal pathogen; isotopic labeling
    DOI:  https://doi.org/10.1128/msystems.00569-25
  6. PLoS One. 2025 ;20(9): e0331582
      Diabetic kidney disease (DKD) involves oxidative stress-driven damage to glomeruli (Gloms) and proximal convoluted tubules (PCT). NAD(P)H: quinone oxidoreductase 1 (NQO1) regulates redox balance, but its compartment-specific role remains unclear. Streptozotocin (STZ)-induced hyperglycemia increased albuminuria and foot process effacement, with NQO1 KO (NKO) mice exhibiting greater podocyte injury than WT, indicating exacerbated glomerular damage. To investigate the underlying mechanisms, we conducted compartment-specific transcriptomic Gene Set Enrichment Analysis (GSEA) in Gloms and PCT. In Gloms, ribosome biogenesis and immune pathways were upregulated in WT-STZ compared to WT but suppressed in NKO-STZ compared to STZ, indicating impaired protein synthesis and immune regulation in NQO1 deficiency. In PCT, ribosome activity, oxidative phosphorylation, glutathione metabolism, and cytoskeletal pathways were elevated in WT-STZ compared to WT but suppressed in NKO-STZ compared to WT-STZ. However, ribosome activity was relatively less affected than in Gloms. Additionally, adherens junction activation was more pronounced in WT-STZ Gloms than in NKO mice Gloms, suggesting a compensatory mechanism to maintain podocyte foot process integrity. This response involved key cytoskeletal genes, including Actg1, Ctnna1, Tjp1, Rhoa, and Iqgap1. These findings highlight compartment-specific adaptive responses to STZ-induced hyperglycemia and underscore NQO1's role in regulating these adaptations. Our results suggest that enhancing NQO1 activity may restore redox balance and preserve nephron integrity, supporting its potential as a therapeutic target for DKD. Furthermore, the observed compartment-specific responses highlight the need for precision redox therapies tailored to glomerular and tubular vulnerabilities.
    DOI:  https://doi.org/10.1371/journal.pone.0331582
  7. Cancer Med. 2025 Sep;14(17): e71225
       BACKGROUND: Prostate cancer is one of the principal malignancies threatening human health, and the development of castration resistance often constitutes a major cause of treatment failure in its management.
    METHODS: To elucidate the potential association between programmed death-ligand 1 (PD-L1) and castration resistance in prostate cancer, we analyzed the expression levels of PD-L1 in both primary prostate cancer tissues and castration-resistant prostate cancer (CRPC) specimens as well as in corresponding cell lines by using western blots and immunohistochemistry. Then, we explored the specific mechanisms through transcriptomic sequencing technology.
    RESULTS: Our findings revealed that, compared to adjacent non-cancerous tissue, PD-L1 expression was unexpectedly lower in primary prostate cancer but notably elevated in CRPC tissues and cells. In CRPC cell lines where PD-L1 was knocked down, a significant suppression of proliferation, invasion, and migration capabilities was observed. By employing next-generation sequencing technology, we investigated the impact of PD-L1 knockdown on intracellular signaling pathways in castration-resistant cells. The results demonstrated that PD-L1 knockdown led to alterations in gene expression within several signaling pathways, including those involved in cell surface interactions, regulation of natural killer cell activity, and sodium channel regulatory activity. We further elucidated through experimentation that PD-L1 contributes to tumor progression in CRPC by modulating the expression of SCUBE1. More intriguingly, PD-L1 knockdown also appeared to induce changes at the level of alternative splicing in multiple genes.
    CONCLUSIONS: PD-L1 is upregulated in CRPC and can modulate the expression of multiple tumor-associated genes in CRPC cells. Finally, we found that PD-L1 contributes to tumor progression in CRPC by modulating the expression of SCUBE1. This study provides a theoretical basis for understanding the intracellular signaling mediated by PD-L1 and offers valuable insights into the mechanisms underlying castration resistance in prostate cancer.
    Keywords:  CRPC; PD‐L1; altinative splicing; prostate cancer; transcriptomic sequencing
    DOI:  https://doi.org/10.1002/cam4.71225
  8. Nutrients. 2025 Sep 04. pii: 2868. [Epub ahead of print]17(17):
      Background: Overweight and obesity are currently a worldwide problem, with undesirable health consequences, such as type 2 diabetes. Therefore, much attention has been paid to preventing obesity through diet. Free fatty acids (FFAs) serve as signaling molecules in many biological processes, leading to increased energy expenditure and insulin secretion. Short-chain fatty acids (SCFAs) such as acetic, propionic and butyric acid are bioactive metabolites produced by gut microbes, and their beneficial effects on host metabolism are well studied. However, the effects of hexanoic acid on metabolism are poorly understood. Methods: Male C57BL/6J mice were fed a normal chow diet, a high-fat diet (HFD), an HFD containing 5% butyric acid or an HFD containing 5% hexanoic acid for 4 weeks, and the effects of hexanoic acid on their lipid and glucose metabolisms were examined. Results: Dietary supplementation of hexanoic acid or butyric acid for 4 weeks prevented HFD-induced obesity and fat accumulation in the white adipose tissues. Both FFAs also suppressed the elevated plasma non-esterified fatty acid (NEFA) levels and hepatic triglyceride content in the mice fed an HFD. In addition, butyric acid and hexanoic acid decreased the elevated expression of genes involved in fatty acid biosynthesis in the white adipose tissues under HFD conditions. Hyperinsulinemia induced by HFD feeding was attenuated by oral intake of butyric acid or hexanoic acid, whereas hyperglycemia under HFD feeding was improved only through oral administration of hexanoic acid. Hexanoic acid increased plasma glucagon-like peptide-1 (GLP-1) levels and the expression of genes associated with gluconeogenesis. The intraperitoneal glucose tolerance test (IPGTT) and the insulin tolerance test (ITT) revealed that the oral administration of hexanoic acid significantly enhanced glucose tolerance and insulin sensitivity. Conclusions: This study highlights the importance of hexanoic acid in improving lipid and glucose metabolisms. Hexanoic acid, as well as butyric acid, is a remarkable FFA with anti-obesity properties. Furthermore, hexanoic acid is more potent in maintaining glucose homeostasis than butyric acid. Thus, our findings provide insight into the development of functional foods which could prevent obesity-related diseases such as type 2 diabetes.
    Keywords:  glucose metabolism; hexanoic acid; insulin resistance; lipid metabolism; obesity
    DOI:  https://doi.org/10.3390/nu17172868
  9. J Biol Chem. 2025 Sep 08. pii: S0021-9258(25)02545-1. [Epub ahead of print] 110693
      Fetal bovine serum (FBS) is an undefined additive that is ubiquitous to mammalian cell culture media and whose functional contributions to promoting cell proliferation remain poorly understood. Efforts to replace serum supplementation in culture media have been hindered by an incomplete understanding of the environmental requirements fulfilled by FBS. Here, we use a combination of live-cell imaging and quantitative lipidomics to elucidate the role of serum in supporting proliferation. We show that serum provides consumed factors that enable proliferation, with serum metal and lipid components serving as crucial metabolic resources. Despite access to a wide range of lipid classes available in serum, we find albumin-bound lipids are the primary species consumed by cancer cells. Furthermore, we find that supplementing with additives that contain necessary metals and any of the albumin-associated lipid classes can obviate the FBS requirement for cancer cell proliferation. Using this defined system, we investigated cancer cell lipid consumption dynamics, finding that albumin-associated lipids are primarily consumed through a mass-action mechanism with minimal competition within or amongst lipid classes. We also find that lipid scavenging is a dominant lipid acquisition route and is necessary for cancer cell proliferation. This work therefore identifies metabolic contributions of serum and provides a framework for building defined culture systems that sustain cell proliferation without the undefined contributions of serum.
    DOI:  https://doi.org/10.1016/j.jbc.2025.110693
  10. Biochem Biophys Rep. 2025 Dec;44 102217
      Breast cancer is the most prevalent cancer among women, posing significant challenges due to its heterogeneity. Recent studies suggest that the ketogenic diet (KD) may enhance chemotherapy efficacy by modulating cancer cell metabolism, particularly through the elevation of ketone bodies like β-hydroxybutyrate (BHB). This study investigates the effects of BHB on breast cancer cells using both 2D and 3D culture models, focusing on its role in developing resistance to fluorouracil (5-FU). We utilized CF41.Mg canine mammary gland cancer cells and MCF7 human breast cancer cells to assess BHB's effects as a pre-treatment and post-treatment under varying glucose conditions. The findings indicated that BHB notably increased cell viability, proliferation, and migration. Pre-treatment resulted in a 52.94 % increase in viability for CF41.Mg cells and a 54.73 % increase for MCF7 cells after 48 h, compared to treatment with 5-FU alone. This enhancement persisted at 72 h, indicating BHB's potential to promote resistance to 5-FU. In 3D spheroid models, which better mimic the tumor microenvironment, BHB pre-treatment significantly increased spheroid size and conferred resistance to 5-FU in both cell lines. Additionally, BHB pre-treatment elevated the expression of proliferation markers such as Ki-67 and tumorigenic markers like MUC-1 (Mucin 1), while showing no significant impact on mesenchymal markers like N-cadherin and vimentin. These findings suggest that BHB significantly increases resistance to 5-FU, indicating that BHB may enable cancer cells to evade chemotherapy-induced stress. Our findings raise important questions about the potential dual role of BHB and KD in promoting cancer cell survival while potentially complicating treatment outcomes.
    Keywords:  Breast cancer; Fluorouracil; Ketogenic diet; Tumorigenesis; β-Hydroxybutyric acid
    DOI:  https://doi.org/10.1016/j.bbrep.2025.102217
  11. Mol Metab. 2025 Sep 10. pii: S2212-8778(25)00155-3. [Epub ahead of print] 102248
      The amino acid composition of the diet has recently emerged as a critical regulator of metabolic health. Consumption of the branched-chain amino acid isoleucine is positively correlated with body mass index in humans, and reducing dietary levels of isoleucine rapidly improves the metabolic health of diet-induced obese male C57BL/6J mice. However, there are some reports that dietary supplementation with extra BCAAs has health benefits. Further, the interactions between sex, genetic background, and dietary isoleucine levels in response to a Western Diet (WD) remain incompletely understood. Here, we find that although the magnitude of the effect varies by sex and strain, reducing dietary levels of isoleucine protects C57BL/6J and DBA/2J mice of both sexes from the deleterious metabolic effects of a WD, while increasing dietary levels of isoleucine impairs aspects of metabolic health. Despite broadly positive responses across all sexes and strains to reduced isoleucine, the molecular response of each sex and strain is highly distinctive. Using a multi-omics approach, we identify a core sex- and strain- independent molecular response to dietary isoleucine, and identify mega-clusters of differentially expressed hepatic genes, metabolites, and lipids associated with each phenotype. Intriguingly, the metabolic effects of reduced isoleucine in mice are not associated with FGF21 - and we find that in humans, plasma FGF21 levels are likewise not associated with dietary levels of isoleucine. Finally, an analysis of human NHANES data shows that isoleucine content varies widely across foods, and that individuals with higher Healthy Eating Index scores tend to consume lower amounts of isoleucine. Our results suggest that the dietary level of isoleucine is a potential mediator of the metabolic and molecular response to a WD, and imply that reducing dietary isoleucine may represent a theoretically translatable strategy to protect from the negative metabolic consequences of a WD.
    Keywords:  Branched-chain amino acids; Isoleucine; adiposity; insulin resistance; metabolic health; western diet
    DOI:  https://doi.org/10.1016/j.molmet.2025.102248