bims-cagime Biomed News
on Cancer, aging and metabolism
Issue of 2025–05–18
thirty-one papers selected by
Kıvanç Görgülü, Technical University of Munich



  1. J Cell Biol. 2025 Jul 07. pii: e202408159. [Epub ahead of print]224(7):
      Microvesicles (MVs) are membrane-enclosed, plasma membrane-derived particles released by cells from all branches of life. MVs have utility as disease biomarkers and may participate in intercellular communication; however, physiological processes that induce their secretion are not known. Here, we isolate and characterize annexin-containing MVs and show that these vesicles are secreted in response to the calcium influx caused by membrane damage. The annexins in these vesicles are cleaved by calpains. After plasma membrane injury, cytoplasmic calcium-bound annexins are rapidly recruited to the plasma membrane and form a scab-like structure at the lesion. In a second phase, recruited annexins are cleaved by calpains-1/2, disabling membrane scabbing. Cleavage promotes annexin secretion within MVs. Our data support a new model of plasma membrane repair, where calpains relax annexin-membrane aggregates in the lesion repair scab, allowing secretion of damaged membrane and annexins as MVs. We anticipate that cells experiencing plasma membrane damage, including muscle and metastatic cancer cells, secrete these MVs at elevated levels.
    DOI:  https://doi.org/10.1083/jcb.202408159
  2. Cell Rep. 2025 May 10. pii: S2211-1247(25)00460-7. [Epub ahead of print]44(5): 115689
      Cancer cachexia is a debilitating metabolic disorder characterized by involuntary loss of body and muscle mass, leading to increased morbidity and mortality. We previously found that forkhead box P1 (FoxP1) upregulation in skeletal muscle causes muscle wasting and is required for muscle wasting in response to cancer. However, transcriptional networks targeted by FoxP1 in skeletal muscles undergoing cancer-induced wasting remain largely unknown. Here, we identify FoxP1 as a key disruptor of the skeletal-muscle clock in response to cancer that reprograms circadian patterns of gene expression at cachexia onset. Specifically, we show that cancer-induced FoxP1 rewires the skeletal-muscle circadian transcriptome toward pathways associated with muscle wasting and disrupts the temporal patterning of pathways governing glucose, lipid, and oxidative metabolism. These findings thus implicate cancer/disease-specific functions of FOXP1 in the disruption and reprograming of the skeletal-muscle circadian transcriptome, which may contribute to muscle wasting and the development of cachexia.
    Keywords:  CP: Cancer; ChIP-seq; RNA-seq; cancer cachexia; circadian rhythm; inflammation; metabolism; muscle atrophy; muscle clock; pancreatic cancer; skeletal muscle
    DOI:  https://doi.org/10.1016/j.celrep.2025.115689
  3. Proc Natl Acad Sci U S A. 2025 May 20. 122(20): e2417024122
      Caveolin is a monotopic integral membrane protein, widely expressed in metazoans 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 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, intercalating into lipid monolayers of various compositions. CAV1-8S can also incorporate into preformed bilayers, but only upon removal of phospholipids from the outer-facing leaflet. Atomistic and coarse-grained simulations of biomimetic bilayers support this "leaflet replacement" model and also reveal that CAV1-8S accumulates 40 to 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. 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.
    Keywords:  Langmuir trough; caveolae; caveolin; lipid–protein interactions; molecular dynamics
    DOI:  https://doi.org/10.1073/pnas.2417024122
  4. Faraday Discuss. 2025 May 12.
      Most eukaryotic cells maintain a large disparity in lipid compositions between the cytosolic and external leaflets of the plasma membrane (PM) bilayer. This lipid asymmetry is maintained by energy-consuming flippase enzymes that selectively drive phospholipids into the cytosolic leaflet, often against large concentration gradients. Scramblases, activated by intracellular Ca2+ or apoptotic signaling, shuttle phospholipids down their concentration gradient to release lipid asymmetry. Such scrambling is typically evidenced by exposure of phosphatidylserine (PS) to the external leaflet and is associated with many physiological processes, most notably blood clotting and cell death, but also activation of immune cells. Here, we show that both PS and phosphatidylethanolamine (PE) appear on the PM external leaflet following immune receptor-mediated activation of mast cells. We also observe similar effects in T cells. Importantly, in contrast to wholesale release of PM asymmetry induced by calcium ionophores or apoptosis, we show that scrambling in activated immune cells is focal, with small, stable regions of surface exposed PS. These scrambled foci are calcium dependent, have lower lipid packing than their surrounding outer leaflet, and are reversible. These observations of local, transient scrambling during physiological activation of healthy immune cells suggest important roles for the lateral and transbilayer organization of membrane lipids.
    DOI:  https://doi.org/10.1039/d4fd00205a
  5. Gut. 2025 May 12. pii: gutjnl-2024-333238. [Epub ahead of print]
       BACKGROUND: RAS mutations are frequently observed in human cholangiocarcinoma (CCA), while they are relatively rare in hepatocellular carcinoma (HCC). The role of RAS-dependent signalling pathways in CCA development is currently not well understood.
    OBJECTIVE: The objective of this study was to investigate RAS-dependent signalling pathways in CCA and their role in tumour development and differentiation.
    DESIGN: We used genetically engineered mouse models with liver-specific deletion of tumour suppressors Rb and p53 together with activation of oncogenic Kras to investigate the cell of origin in intrahepatic CCA and to elucidate the role of RAS-dependent signalling pathways in CCA development.
    RESULTS: In mice, Kras-mutant intrahepatic CCA develops primarily from hepatocytes and shows activation of PI3K/AKT and MEK/ERK signalling downstream of KRAS. Targeted genetic inactivation of each of these pathways leads to delayed tumour growth and profound alterations in tumour differentiation. Specifically, reduced PI3K/AKT signalling promotes more well-differentiated tumours, whereas the inactivation of MEK/ERK signalling induces a differentiation switch towards a more hepatocyte-like phenotype. This switch is accompanied by activation of WNT/β-catenin signalling, a pathway commonly activated in human HCC.
    CONCLUSIONS: These findings provide insights into the role of RAS-dependent pathways in liver cancer differentiation and offer a compelling explanation for the high prevalence of RAS mutations in human CCA compared with HCC.
    Keywords:  CANCER GENETICS; CHOLANGIOCARCINOMA; HEPATOBILIARY CANCER
    DOI:  https://doi.org/10.1136/gutjnl-2024-333238
  6. Nat Genet. 2025 May;57(5): 1189-1200
    Cancer Genome Atlas Analysis Network
      Genome conformation underlies transcriptional regulation by distal enhancers, and genomic rearrangements in cancer can alter critical regulatory interactions. Here we profiled the three-dimensional genome architecture and enhancer connectome of 69 tumor samples spanning 15 primary human cancer types from The Cancer Genome Atlas. We discovered the following three archetypes of enhancer usage for over 100 oncogenes across human cancers: static, selective gain or dynamic rewiring. Integrative analyses revealed the enhancer landscape of noncancer cells in the tumor microenvironment for genes related to immune escape. Deep whole-genome sequencing and enhancer connectome mapping provided accurate detection and validation of diverse structural variants across cancer genomes and revealed distinct enhancer rewiring consequences from noncoding point mutations, genomic inversions, translocations and focal amplifications. Extrachromosomal DNA promoted more extensive enhancer rewiring among several types of focal amplification mechanisms. These results suggest a systematic approach to understanding genome topology in cancer etiology and therapy.
    DOI:  https://doi.org/10.1038/s41588-025-02188-0
  7. Cell Metab. 2025 May 08. pii: S1550-4131(25)00253-0. [Epub ahead of print]
      Cold exposure is a selective environmental stress that elicits a rapid metabolic shift to maintain energy homeostasis. In response to cold exposure, the liver rewires the metabolic state, shifting from glucose to lipid catabolism. By probing the liver lipids in cold exposure, we observed that the lysosomal bis(monoacylglycero)phosphate (BMP) lipids were rapidly increased during cold exposure. BMP lipid changes occurred independently of lysosomal abundance but were dependent on the lysosomal transcriptional regulator transcription factor EB (TFEB). Knockdown of Tfeb in hepatocytes decreased BMP lipid levels and led to cold intolerance in mice. We assessed TFEB-binding sites of lysosomal genes and determined that the phospholipase a2 group XV (PLA2G15) regulates BMP lipid catabolism. Decreasing Pla2g15 levels in mice increased BMP lipids, ablated the cold-induced rise in BMP lipids, and improved cold tolerance. Mutation of the catalytic site of PLA2G15 ablated the BMP lipid breakdown. Together, our studies uncover TFEB regulation of BMP lipids through PLA2G15 catabolism.
    Keywords:  BMP; LC-MS; Pla2g15; TFEB; bis(monoacylglycero)phosphate; cold exposure; lipidomics; liquid chromatography-mass spectrometry; liver; lysosome; phospholipase A2 G15; transcription factor EB
    DOI:  https://doi.org/10.1016/j.cmet.2025.04.015
  8. J Cell Physiol. 2025 May;240(5): e70044
      Lysosomes are essential organelles degrading a wide range of substrates, maintaining cellular homeostasis, and regulating cell growth through nutrient and metabolic signaling. A key vulnerability of lysosomes is their membrane permeabilization (LMP), a process tightly linked to diseases including aging, neurodegeneration, lysosomal storage disorders, and cardiovascular disease. Research progress in the past few years has greatly improved our understanding of lysosomal repair mechanisms. Upon LMP, cells activate multiple membrane remodeling processes to restore lysosomal integrity, such as membrane invagination, tubulation, lipid patching, and membrane stabilization. These repair pathways are critical in preserving cellular stress tolerance and preventing deleterious inflammation and cell death triggered by lysosomal damage. This review focuses on the expanding mechanistic insights of lysosomal repair, highlighting its crucial role in maintaining cellular health and the implications for disease pathogenesis and therapeutic strategies.
    Keywords:  Atg8ylation; CASM; ESCRT; Lysosomal repair; PITT; annexins; lysosomal membrane permeabilization; microlysophagy; stress granules
    DOI:  https://doi.org/10.1002/jcp.70044
  9. Int J Mol Sci. 2025 Apr 28. pii: 4193. [Epub ahead of print]26(9):
      Despite centuries of research, metastatic cancer remains incurable due to resistance to all conventional cancer therapeutics. Alternative strategies leveraging non-proliferative vulnerabilities in cancer are required to overcome cancer recurrence. Ferroptosis is an iron dependent cell death pathway that has shown promising pre-clinical activity in several contexts of therapeutic resistant cancer. However, ferroptosis sensitivity is highly variable across tissue types and cell states, posing a challenge for clinical translation. We describe a convergent phenotype induced by chemotherapy where cells surviving chemotherapy have dysregulated iron homeostasis, regardless of initial cell type or chemotherapy used. Elevated labile iron levels are counteracted by NRF2 signaling, yet the resulting antioxidant programs do not alleviate the labile iron burden. Selectively inhibiting GPX4 leads to uniform susceptibility to ferroptosis in surviving cells, highlighting the common reliance on lipid peroxidation defenses. Cellular iron dysregulation is a vulnerability of chemoresistant cancer cells that can be leveraged by triggering ferroptosis.
    Keywords:  chemotherapy; ferroptosis; labile iron; therapeutic resistance
    DOI:  https://doi.org/10.3390/ijms26094193
  10. J Clin Oncol. 2025 May 12. JCO2301965
       PURPOSE: This randomized phase-II trial (ClinicalTrials.gov identifier: NCT02767557) compared efficacy of gemcitabine/nab-paclitaxel (Gem/Nab) with or without the anti-interleukin-6 (IL-6) receptor antibody tocilizumab (Toc) for advanced pancreatic cancer (PC).
    METHODS: A safety cohort received Gem 1,000 mg/m2 and Nab 125 mg/m2 on days 1, 8, and 15, and Toc 8 mg/kg on day 1 for each 28-day cycle. Participants with modified Glasgow prognostic scores of 1 or 2 were randomly assigned 1:1 to receive Gem/Nab/Toc or Gem/Nab. The primary end point was the overall survival (OS) rate at 6 months (OS6). Secondary end points were progression-free survival (PFS), overall response rate (ORR), and safety. Exploratory end points were cachexia, quality of life, and biomarkers, including the cachexia-promoting protein, growth differentiation factor 15 (GDF15).
    RESULTS: Overall, 147 patients were treated, including six safety cohort participants. The median follow-up period was 8.1 months (IQR, 4.2-13.9). OS6 was 68.6% (95% CI, 56.3 to 78.1) for the Gem/Nab/Toc group and 62.0% (49.6-72.1) for the Gem/Nab group (P = .409). OS for Gem/Nab/Toc versus Gem/Nab improved at 18 months (27.1% v 7.0%, P = .001). No differences in median OS, PFS, or ORR were observed. Incidence of grade-3+ treatment-related adverse events (TrAEs) was 88.1% for Gem/Nab/Toc and 63.4% for Gem/Nab (P < .001). Gem/Nab/Toc decreased muscle loss versus Gem/Nab, with median change +0.1013% versus -3.430% (P = .0012) at 2 months and +0.7044 versus -3.353% (P = .036) at 4 months. Incidence of muscle loss was 43.48% on Gem/Nab/Toc versus 73.52% on Gem/Nab at 2 months (P = .0045) and 41.82% versus 68.75% (P = .0062) at 4 months. GDF15 was not changed by Gem/Nab or Gem/Nab/Toc.
    CONCLUSION: Although the primary end point was not met and TrAEs were increased by Toc, increased survival at 18 months and reduced muscle wasting support an anticachexia effect of IL-6 blockade independent of GDF15. Further studies could leverage these findings for precision anticachexia therapy.
    DOI:  https://doi.org/10.1200/JCO.23.01965
  11. Mol Cancer Res. 2025 May 16.
      TRAP1, the mitochondrial isoform of HSP90, has emerged as a key regulator of cancer cell metabolism, yet the mechanisms by which it rewires nutrient utilization remain poorly understood. We previously reported that TRAP1 loss increases glutamine dependency of mitochondrial respiration following glucose withdrawal. Here, we investigate how TRAP1 deletion impacts glucose metabolism and the mechanisms enabling glutamine retention to support mitochondrial respiration via reductive carboxylation and the oxidative TCA cycle. TRAP1 knockout (KO) in bladder and prostate cancer cells recapitulates the carbon source-specific metabolic rewiring previously observed. Stable isotope tracing reveals that although glucose oxidation remains functional, TRAP1 KO reduces overall glucose uptake and its contribution to glycolysis and the pentose phosphate pathway. This effect is consistent across multiple cell lines. Concurrently, TRAP1-deficient cells exhibit increased glutamine retention and reliance, potentially due to downregulation of the cystine/glutamate antiporter SLC7A11/xCT. Supporting this, xCT overexpression reduces glutamine-dependent respiration in TRAP1 KO cells. qPCR and proteasome inhibition assays suggest xCT is regulated post-translationally via protein stability. Notably, xCT suppression does not trigger ferroptosis, indicating a selective adaptation rather than induction of cell death. Together, our findings suggest that TRAP1 loss decreases glucose uptake while preserving its metabolic fate, promoting glutamine conservation through xCT downregulation to maintain mitochondrial respiration without inducing ferroptosis. Implications: These results reveal a TRAP1-dependent mechanism of metabolic rewiring in cancer cells and identify xCT-mediated glutamine conservation as a key adaptive response, underscoring TRAP1 as a potential metabolic vulnerability and therapeutic target in tumors with altered nutrient utilization.
    DOI:  https://doi.org/10.1158/1541-7786.MCR-24-0194
  12. Autophagy. 2025 May 14. 1-3
      Aggregates of polyglutamine (polyQ) repeat extensions are known markers of several, predominantly inherited, neurodegenerative diseases. Removal of polyQ is essential for cellular proteostasis and macroautophagy/autophagy has been proposed to be an important tool in the clearance of polyQ aggregates. The mechanism of recognition and encapsulation of these aggregates within autophagosomes is largely unknown. A study described in this article employed in situ correlative cryo-electron tomography to visualize polyQ aggregates interacting with autophagic compartments. The tomograms revealed that only amorphous polyQ, but not fibrils, are engulfed by double-membrane structures and that SQSTM1/p62 is the receptor involved in recognition of polyQ during autophagy. Solidified amorphous polyQ and subsequent fibrils arrest the normal formation of autophagosomes and impair autophagy. Findings of the study described here have implications for therapies that rely on autophagy in targeting polyQ neurodegeneration.Abbreviation: cryo-CLEM, cryo-correlative light and electron microscopy; cryo-ET, cryo-electron tomography; ER, endoplasmic reticulum; HD, Huntington disease; HTT, huntingtin; polyQ, polyglutamine repeats.
    Keywords:  Amorphous phase; SQSTM1/p62; cryo-electron tomography, fibrillar phase; huntingtin; neurodegeneration
    DOI:  https://doi.org/10.1080/15548627.2025.2503578
  13. NPJ Syst Biol Appl. 2025 May 10. 11(1): 46
      Abnormal metabolism is a hallmark of cancer, this was initially recognized nearly a century ago through the observation of aerobic glycolysis in cancer cells. Mitochondrial respiration can also drive tumor progression and metastasis. However, it remains largely unclear the mechanisms by which cancer cells mix and match different metabolic modalities (oxidative/reductive) and leverage various metabolic ingredients (glucose, fatty acids, glutamine) to meet their bioenergetic and biosynthetic needs. Here, we formulate a phenotypic model for cancer metabolism by coupling master gene regulators (AMPK, HIF-1, MYC) with key metabolic substrates (glucose, fatty acids, and glutamine). The model predicts that cancer cells can acquire four metabolic phenotypes: a catabolic phenotype characterized by vigorous oxidative processes-O, an anabolic phenotype characterized by pronounced reductive activities-W, and two complementary hybrid metabolic states-one exhibiting both high catabolic and high anabolic activity-W/O, and the other relying mainly on glutamine oxidation-Q. Using this framework, we quantified gene and metabolic pathway activity by developing scoring metrics based on gene expression. We validated the model-predicted gene-metabolic pathway association and the characterization of the four metabolic phenotypes by analyzing RNA-seq data of tumor samples from TCGA. Strikingly, carcinoma samples exhibiting hybrid metabolic phenotypes are often associated with the worst survival outcomes relative to other metabolic phenotypes. Our mathematical model and scoring metrics serve as a platform to quantify cancer metabolism and study how cancer cells adapt their metabolism upon perturbations, which ultimately could facilitate an effective treatment targeting cancer metabolic plasticity.
    DOI:  https://doi.org/10.1038/s41540-025-00525-x
  14. Trends Cancer. 2025 May 14. pii: S2405-8033(25)00121-9. [Epub ahead of print]
      Despite significant milestones in cancer immunotherapy, tumor cells often escape immune surveillance. Zhou et al. revealed that the pivotal ferroptosis suppressor glutathione peroxidase 4 (GPX4) can undergo palmitoylation by zDHHC8, enhancing ferroptosis resistance. This study highlights the potential of targeting GPX4 palmitoylation to enhance cytotoxic T cell-mediated ferroptosis of tumor cells.
    Keywords:  GPX4; ferroptosis; immune-checkpoint blockade (ICB); palmitoylation; tumor microenvironment (TME); zDHHC8
    DOI:  https://doi.org/10.1016/j.trecan.2025.05.001
  15. Biophys Rev. 2025 Apr;17(2): 591-604
      Membrane-active peptides (MAPs) are versatile molecules that interact with lipid bilayers, facilitating processes such as antimicrobial defense, anticancer activity, and membrane translocation. Given that most MAPs are cationic, their selectivity for specific cell membranes has traditionally been attributed to variations in membrane surface charge. However, growing evidence suggests that electrostatics alone cannot fully explain MAPs selectivity. Instead, MAPs activity is also strongly influenced by other membrane biophysical properties, such as lipid packing, phase state, curvature, and the spatial distribution of hydrophobic and charged residues within the peptide sequence. In this review, we summarize the current knowledge on the biophysical determinants of MAPs selectivity. We begin by examining membrane and cell surface electrostatics and their influence on MAPs-membrane interactions, including electrostatically driven peptide conformational changes and lipid recruitment. We then broaden the discussion to include non-electrostatic factors, such as membrane curvature and rheology, which are primarily influenced by sterol or hopanoid content, as well as acyl chain unsaturation and branching. Together, these processes highlight that MAPs selectivity is not governed by any single membrane property but instead emerges from a synergistic interplay of electrostatic, hydrophobic, and topological factors.
    Supplementary Information: The online version contains supplementary material available at 10.1007/s12551-025-01309-7.
    Keywords:  Arginine; Hopanoids; Sterols; Zeta potential of cells; pH-regulated activity
    DOI:  https://doi.org/10.1007/s12551-025-01309-7
  16. Nature. 2025 May 14.
      The anti-tumour effect of radiotherapy beyond the treatment field-the abscopal effect-has garnered much interest1. However, the potentially deleterious effect of radiation in promoting metastasis is less well studied. Here we show that radiotherapy induces the expression of the EGFR ligand amphiregulin in tumour cells, which reprogrammes EGFR-expressing myeloid cells toward an immunosuppressive phenotype and reduces phagocytosis. This stimulates distant metastasis growth in human patients and in pre-clinical mouse tumour models. The inhibition of these tumour-promoting factors induced by radiotherapy may represent a novel therapeutic strategy to improve patient outcomes.
    DOI:  https://doi.org/10.1038/s41586-025-08994-0
  17. Nat Immunol. 2025 May 12.
      The benefit of immune checkpoint blockade for cancer therapy is limited to subsets of patients because of factors including the accumulation of immunosuppressive metabolites, such as adenosine, within tumors. Pharmacological inhibition of adenosine generation and signaling is an active area of clinical investigation, but only limited clinical benefit has been reported. Here, we show that adenosine suppresses anti-cancer T cell responses following uptake into activated T cells by equilibrative nucleoside transporter 1 (ENT1) and inhibition of de novo pyrimidine nucleotide synthesis. We identify EOS301984 as a potent ENT1 antagonist that restores pyrimidine levels in activated T cells in adenosine-rich environments, resulting in enhanced tumor cell killing by memory T cells and increased ex vivo expansion of functional human tumor-infiltrating lymphocytes. A combination of EOS301984 with anti-PD-1 led to synergistic control of tumor growth in a humanized mouse model of triple-negative breast cancer. ENT1 inhibition, therefore, augments anti-cancer immune responses through the restoration of pyrimidine nucleotide synthesis in T cells suppressed by adenosine.
    DOI:  https://doi.org/10.1038/s41590-025-02153-3
  18. Proc Natl Acad Sci U S A. 2025 May 20. 122(20): e2426179122
      Mitochondrial energy metabolism is vital for muscle function and is tightly controlled at the transcriptional level, both in the basal state and during adaptive muscle remodeling. The importance of the transcription factors estrogen-related receptors (ERRs) in controlling innate mitochondrial energetics has been recently demonstrated. However, whether different ERR isoforms display distinct functions in glycolytic versus oxidative myofibers is largely unknown. Moreover, their roles in regulating exercise-induced adaptive mitochondrial biogenesis remain unclear. Using muscle-specific single and combinatorial knockout mouse models, we have identified both cooperative and distinct roles of the ERR isoforms ERRα and ERRγ in regulating mitochondrial energy metabolism in different muscles. We demonstrate the essential roles of both these ERRs in mediating adaptive mitochondrial biogenesis in response to exercise training. We further show that PGC1α-induced mitochondrial biogenesis is completely abolished in primary myotubes with ERRα deletion but not ERRγ, highlighting distinct roles of these two isoforms in adaptive mitochondrial remodeling. Mechanistically, we find that both ERRs directly bind to the majority of mitochondrial energetic genes and control their expression, largely through collaborative binding to the same genomic loci. Collectively, our findings reveal critical and direct regulatory roles of ERRα and ERRγ in governing both innate and adaptive mitochondrial energetics in skeletal muscle.
    Keywords:  PGC1; energy metabolism; estrogen-related receptor; mitochondria; muscle
    DOI:  https://doi.org/10.1073/pnas.2426179122
  19. Biochim Biophys Acta Mol Cell Biol Lipids. 2025 May 10. pii: S1388-1981(25)00033-2. [Epub ahead of print] 159625
      How lipids are sorted between intracellular compartments and what mechanisms support inter-organellar lipid transport define questions that have enjoyed long-standing interest in the cell biology community. Despite tantalizing evidence to the effect that lipids can move between organelles independently of standard modes of vesicular membrane trafficking through the secretory pathway, biochemical dissection of these non-vesicular pathways was initially fraught with experimental challenges. Many of the obstacles have now been overcome and, following initial breakthroughs, the last two decades have witnessed a renaissance in the field of lipid trafficking. Indeed, lipid trafficking and mobilization are now significant components of any discussion regarding secretory vesicle trafficking, organelle biogenesis, agonist-stimulated lipid signaling, and inter-compartmental communication pathways that involve every organelle in the eukaryotic cell. In accord with the theme of this special issue, we focus on the topic of soluble lipid transfer proteins that interface with the metabolism of phosphatidylinositol (PtdIns) and its phosphorylated derivatives - the phosphoinositides. Although phosphoinositides are quantitatively minor lipids in cells, these molecules represent the chemical codes for a major pathway of intracellular signaling in all eukaryotic cells. It is now clear that soluble PtdIns transfer proteins (PITPs) are physiologically critical regulators of specific pathways of phosphoinositide - particularly PtdIns-4-phosphate - signaling. The 'where' PITPs determine the biological outcomes of phosphoinositide signaling, and the 'how' by which PITPs do so, represent increasingly active areas of research in contemporary cell biology. It is these issues we explore from a historical perspective with a focus on the Sec14-like PITPs.
    Keywords:  Anti-fungal compounds; Lipid signaling; Phosphatidylinositol transfer proteins; Phosphoinositides
    DOI:  https://doi.org/10.1016/j.bbalip.2025.159625
  20. Sci Adv. 2025 May 16. 11(20): eado3440
      The PPP1R3B gene, encoding PPP1R3B protein, is critical for liver glycogen synthesis and maintaining blood glucose levels. Genetic variants affecting PPP1R3B expression are associated with several metabolic traits and liver disease, but the precise mechanisms are not fully understood. We studied the effects of both Ppp1r3b overexpression and deletion in mice and cell models and found that both changes in Ppp1r3b expression result in dysregulated metabolism and liver damage, with overexpression increasing liver glycogen stores, while deletion resulted in higher liver lipid accumulation. These patterns were confirmed in humans where variants increasing PPP1R3B expression had lower liver fat and decreased plasma lipids, whereas putative loss-of-function variants were associated with increased liver fat and elevated plasma lipids. These findings support that PPP1R3B is a crucial regulator of hepatic metabolism beyond glycogen synthesis and that genetic variants affecting PPP1R3B expression levels influence if hepatic energy is stored as glycogen or triglycerides.
    DOI:  https://doi.org/10.1126/sciadv.ado3440
  21. Semin Cancer Biol. 2025 May 08. pii: S1044-579X(25)00059-8. [Epub ahead of print]
      Diagnosis and treatment of cancer constitute a deeply stressful experience that involves unique and common problems and generates uncertainty, fear and emotional distress. Furthermore, there are reciprocal interactions between psychological stress and cancer in the clinical settings. Therefore, it is crucial to understand the links of stress with cancer. A growing body of epidemiological and preclinical studies have suggested that stress affects cancer progression, and metastasis and treatment outcomes. Furthermore, stress elicits premature aging and deterioration of the immune system (known as immunosenescence), causing vulnerability to infections, autoimmune diseases, and cancers. In this review, we describe recent advances in how stress affects cancer progression through specific stress hormones and receptor systems as well as intracellular molecular processes, and discuss how stress-evoked neuroendocrine molecules regulate local and systemic immune responses in the tumor microenvironment. Furthermore, we review the molecular mechanisms of immunosenescence and evidence of psychological stress-evoked immunosenescence, highlighting the clinical value for available psychological and/or pharmacological interventions for psychological stress in patients with cancer. Based on existing evidence and emerging mechanistic insights, factors linked with psychological stress, immunosenescence and complications in cancer survivors need to be determined in future studies, and screening programs should be added to follow-up.
    Keywords:  aging; cancer survivors; immunosenescence; psychological stress; treatment
    DOI:  https://doi.org/10.1016/j.semcancer.2025.05.007
  22. J Cell Sci. 2025 May 01. pii: jcs263757. [Epub ahead of print]138(9):
      Mitochondria are metabolic hubs that are essential for cellular homeostasis. Most mitochondrial proteins are translated in the cytosol and imported into the organelle. However, import machineries can become overwhelmed or disrupted by physiological demands, mitochondrial damage or diseases, such as metabolic and neurodegenerative disorders. Impaired import affects mitochondrial function and causes un-imported pre-proteins to accumulate not only in the cytosol but also in other compartments, including the endoplasmic reticulum and nucleus. Quality control pathways have evolved to mitigate the accumulation of these mistargeted proteins and prevent proteotoxicity. In this Cell Science at a Glance article and the accompanying poster, we summarize the fate of un-imported mitochondrial proteins and the compartment-specific quality control pathways that regulate them.
    Keywords:  Mitochondrial protein import; Mitochondrial stress; Protein quality control
    DOI:  https://doi.org/10.1242/jcs.263757
  23. J Cell Mol Med. 2025 May;29(9): e70608
      The appearance of hybrid epithelial-mesenchymal (E/M) cells expressing E-cadherin is favourable for the establishment of pro-invasive function. Although the potential role of E-cadherin in cancer invasion is now accepted, the molecular mechanisms involved in this process are not completely elucidated. To gain further insight, we focused our analysis on invadopodia formation, an early event in the invasion process. We used models of E/M hybrid cell lines, tissue sections and patient-derived xenografts from a multi-centre clinical trial. E-cadherin involvement in invadopodia formation was assessed using a gelatin-FITC degradation assay. Mechanistic studies were performed by using proteomic analysis, siRNA strategy and proximity ligation assay. We showed that E-cadherin is a critical component of invadopodia. This unexpected localization results from a synergistic trafficking of E-cadherin and MT1-MMP through a Rab vesicle-dependent pathway. Modulation of E-cadherin expression or activation impacted invadopodia formation. Moreover, colocalization of E-cadherin and Actin in "ring structures" as precursors of invadopodia reveals that E-cadherin is required for invadopodia structuration. E-cadherin, initially localised in the adherens junctions, could be recycled to nascent invadopodia where it will interact with several components enriched in invadopodia, such as Arp2/3, Cortactin or MT1-MMP. The trans-adhesive properties of E-cadherin are therefore essential for structuring invadopodia. This new localisation of E-cadherin and its unexpected role in cell invasion shine a new light on hybrid E/M transition features in tumoral invasion.
    Keywords:  EMT hybrid cells; adhesion molecules; cell invasion; matrix degradation
    DOI:  https://doi.org/10.1111/jcmm.70608
  24. Nat Methods. 2025 May 13.
      The subcellular localization of a protein is important for its function, and its mislocalization is linked to numerous diseases. Existing datasets capture limited pairs of proteins and cell lines, and existing protein localization prediction models either miss cell-type specificity or cannot generalize to unseen proteins. Here we present a method for Prediction of Unseen Proteins' Subcellular localization (PUPS). PUPS combines a protein language model and an image inpainting model to utilize both protein sequence and cellular images. We demonstrate that the protein sequence input enables generalization to unseen proteins, and the cellular image input captures single-cell variability, enabling cell-type-specific predictions. Experimental validation shows that PUPS can predict protein localization in newly performed experiments outside the Human Protein Atlas used for training. Collectively, PUPS provides a framework for predicting differential protein localization across cell lines and single cells within a cell line, including changes in protein localization driven by mutations.
    DOI:  https://doi.org/10.1038/s41592-025-02696-1
  25. Nat Photonics. 2025 ;19(5): 494-501
      Brillouin microscopy is an emerging optical elastography technique that can be used to assess mechanical properties of biological samples in a three-dimensional, all-optical and hence non-contact fashion. However, the low cross-section of spontaneous Brillouin scattering produces weak signals that often necessitate prolonged exposure times or illumination dosages that are potentially harmful for biological samples. Here we present a new approach for highly multiplexed and therefore rapid spectral acquisition of the Brillouin-scattered light. Specifically, by exploiting a custom-built Fourier-transform imaging spectrometer and the symmetric properties of the Brillouin spectrum, we experimentally demonstrate full-field 2D spectral Brillouin imaging of phantoms as well as biological samples, at a throughput of up to 40,000 spectra per second, with a precision of ~70 MHz and an effective 2D image acquisition speed of 0.1 Hz over a ~300 × 300 µm2 field of view. This represents an approximately three-orders-of-magnitude improvement in speed and throughput compared with standard confocal methods, while retaining high spatial resolution and the capability to acquire three-dimensional images of photosensitive samples in biology and medicine.
    Keywords:  Microscopy; Optical spectroscopy
    DOI:  https://doi.org/10.1038/s41566-025-01619-y
  26. Oncologist. 2025 May 08. pii: oyaf083. [Epub ahead of print]30(5):
       INTRODUCTION: In the current study, we aimed to assess the efficacy of a gemcitabine response predictive signature that is part of the PancreasView transcriptomic predictive tool (Gem + or Gem-).
    METHODS: We used a cohort of pancreatic ductal adenocarcinoma patients treated from the Massachusetts General Hospital who underwent upfront resection.
    RESULTS: In this cohort of 43 patients, 20 (46.5%) received adjuvant gemcitabine (GEM arm) and 23 (53.5%) did not receive any adjuvant chemotherapy. Among the 43 patients, the Gem signature defined a subgroup of 16 patients (37.2%) who were sensitive (Gem+) and 27 (62.8%), who were resistant to gemcitabine (Gem-). The Gem+ patients who received adjuvant gemcitabine had significantly better median disease-free survival (DFS) compared to the Gem- patients (NR until 72 months of follow-up vs 19.0 months; stratified hazard ratio [HR]: 0.19; 95% CI, 0.04-0.86; P = .032) and longer median cancer-specific survival (CSS) (NR until 96 months of follow-up vs 37.0 months; stratified HR: 0.18; 95% CI, 0.04-0.85; P = .030) when treated with gemcitabine. The gemcitabine signature remained an independent predictive factor for DFS (HR: 0.41; 95% CI, 0.19-0.89; P = .024) and CSS (HR: 0.47; 95% CI, 0.22-1.23; P = .059) after adjusting for clinicopathological characteristics in an unstratified univariate Cox hazard model.
    CONCLUSIONS: This validation of the gemcitabine predictive transcriptomic signature in an independent cohort from Massachusetts General Hospital reinforces the robustness and reliability of this tool. This study highlights the potential of the signature to aid in the personalization of chemotherapy and enhance patient outcomes in pancreatic ductal adenocarcinoma.
    Keywords:   PancreasView ; PDAC; clinical trial; personalized treatment; transcriptomic signatures
    DOI:  https://doi.org/10.1093/oncolo/oyaf083
  27. J Lipid Res. 2025 May 09. pii: S0022-2275(25)00084-7. [Epub ahead of print] 100824
      Stearoyl-CoA desaturase-1 (SCD1) is a critical regulator of lipogenesis that catalyzes the synthesis of monounsaturated fatty acids (MUFA), mainly oleate (18:1n-9) and palmitoleate (16:1n-7) from saturated fatty acids (SFA), stearoyl-CoA (18:0) and palmitoyl-CoA (16:0), respectively. Elevated SCD1 expression and its products are associated with obesity, metabolic dysfunction-associated steatotic liver disease, insulin resistance, and cancer. Conversely, Scd1 deficiency diminishes de novo lipogenesis and protects mice against adiposity, hepatic steatosis, and hyperglycemia. Yet, the comprehensive impact of Scd1 deficiency on hepatic and circulating lipids remains incompletely understood. To further delineate the effects of SCD1 on lipid metabolism, we employed lipidomics on the liver from mice under a lipogenic high carbohydrate, very low-fat diet. We found that Scd1 deficiency leads to an accumulation of saturated lipids and an increase in hepatic and plasma acylcarnitines. Remarkably, transgenic replenishment of de novo oleate synthesis by human SCD5 in the liver of Scd1-deficient mice not only restored hepatic lipid desaturation levels but also attenuated acylcarnitine accumulation, highlighting the distinct role of SCD1 and oleate in regulating intracellular lipid homeostasis.
    Keywords:  Acylcarnitines; SCD1; SCD5; SFA; lipidomics; oleate
    DOI:  https://doi.org/10.1016/j.jlr.2025.100824
  28. J Clin Oncol. 2025 May 16. JCO2402210
       PURPOSE: More than 30% of patients with pancreatic cancer are unresectable because of the local extension with a median overall survival (OS) of <1 year. Combination of fluorouracil (FU), oxaliplatin, and irinotecan (FOLFIRINOX) is superior to gemcitabine in the treatment of metastatic pancreatic cancer, but standard of care remains gemcitabine in locally advanced pancreatic cancer (LAPC).
    METHODS: Patients with histologically proven LAPC not suitable for surgery, Eastern Cooperative Oncology Group WHO performance status (PS) ≤1 were eligible. Random assignment was stratified by center, tumor localization (pancreas head yes/no), WHO PS (0 v 1), and age (≤60 years v >60 years). Patients received FOLFIRINOX or gemcitabine for 6 months. The primary end point was progression-free survival (PFS). Main secondary end points were OS, time to treatment failure, quality of life, and safety. One hundred seventy patients (142 events) were needed to detect an increase of 3 months in PFS with 80% power (log-rank test, 5% two-sided α).
    RESULTS: One hundred seventy one patients age 35-84 years were included and followed for a maximum of 5 years. With a median follow-up of 59.6 months (95% CI, 42.3 to not reached), 168 events were observed and the median PFS was 9.7 months (95% CI, 7.0 to 11.7) with FOLFIRINOX versus 7.7 months (95% CI, 6.2 to 9.2) with gemcitabine, hazard ratio (HR), 0.7 (95% CI, 0.5 to 1.0), P = .04. The median OS was 15.7 months (95% CI, 11.9 to 20.4) in the FOLFIRINOX group versus 15.4 months (95% CI, 11.7 to 18.6) in the gemcitabine group, HR, 1.02 (95% CI, 0.73 to 1.43), P = .95.
    CONCLUSION: Results confirm that FOLFIRINOX improves PFS significantly compared with gemcitabine and is well tolerated in LAPC. No significant difference in OS was observed between both groups.
    DOI:  https://doi.org/10.1200/JCO-24-02210