bims-cagime Biomed News
on Cancer, aging and metabolism
Issue of 2026–01–11
thirty-six papers selected by
Kıvanç Görgülü, Technical University of Munich



  1. Nat Cell Biol. 2026 Jan 07.
      Changes in cell state are often accompanied by altered metabolic demands, and homeostasis depends on cells adapting to their changing needs. One major cell state change is senescence, which is associated with dramatic changes in cell metabolism, including increases in lipid metabolism, but how cells accommodate such alterations is poorly understood. Here we show that the transcription factor p53 increases recycling of the lipid headgroups required to meet the increased demand for membrane phospholipids during senescence. p53 activation increases the supply of phosphoethanolamine, an intermediate in the Kennedy pathway for de novo synthesis of phosphatidylethanolamine, in part by increasing lipid turnover and transactivating genes involved in autophagy and lysosomal catabolism that enable membrane turnover. Disruption of phosphoethanolamine conversion to phosphatidylethanolamine is well tolerated in the absence of p53 but results in dramatic organelle remodelling and perturbs growth and gene expression following p53 activation. Consistently, CRISPR-Cas9-based genetic screens reveal that p53-activated cells preferentially depend on genes involved in lipid metabolism and lysosomal function. Together, these results reveal lipid headgroup recycling to be a homeostatic function of p53 that confers a cell-state-specific metabolic vulnerability.
    DOI:  https://doi.org/10.1038/s41556-025-01853-0
  2. Nature. 2026 Jan 07.
      Cancer metastasis is a major contributor to patient morbidity and mortality1, yet the factors that determine the organs where cancers can metastasize are incompletely understood. Here we quantify the absolute levels of 124 metabolites in multiple tissues in mice and investigate how this relates to the ability of breast cancer cells to grow in different organs. We engineered breast cancer cells with broad metastatic potential to be auxotrophic for specific nutrients and assessed their ability to colonize different tissue sites. We then asked how tumour growth in different tissues relates to nutrient availability and tumour biosynthetic activity. We find that single nutrients alone do not define the sites where breast cancer cells can grow as metastases. In addition, we identify purine synthesis as a requirement for tumour growth and metastasis across many tissues and find that this phenotype is independent of tissue nucleotide availability or tumour de novo nucleotide synthesis activity. These data suggest that a complex interplay between multiple nutrients within the microenvironment dictates potential sites of metastatic cancer growth, and highlights the interdependence between extrinsic environmental factors and intrinsic cellular properties in influencing where breast cancer cells can grow as metastases.
    DOI:  https://doi.org/10.1038/s41586-025-09898-9
  3. Nat Chem Biol. 2026 Jan 07.
      Cellular lipid metabolism is subject to strong homeostatic regulation, but the players involved in and mechanisms underlying these pathways remain largely uncharacterized. Here we develop a 'feeding-fishing' approach coupling membrane editing using optogenetic lipid-modifying enzymes (feeding) with organelle membrane proteomics through proximity labeling (fishing) to elucidate molecular players and pathways involved in the homeostasis of phosphatidic acid (PA), a multifunctional lipid central to glycerolipid metabolism. This approach identified several PA-metabolizing enzymes and lipid transfer proteins enriched in and depleted from PA-fed membranes. Mechanistic analysis revealed that PA homeostasis in the cytosolic leaflets of the plasma membrane and lysosomes is mediated by both local PA metabolism and the action of lipid transfer proteins that carry out interorganelle lipid transport before subsequent metabolism. More broadly, the interfacing of membrane editing to controllably modify membrane lipid composition with organelle membrane proteomics using proximity labeling represents a strategy for revealing mechanisms governing lipid homeostasis.
    DOI:  https://doi.org/10.1038/s41589-025-02104-x
  4. Nature. 2026 Jan 07.
      Lipid transfer proteins (LTPs) maintain the specialized lipid compositions of organellar membranes1,2. In humans, many LTPs are implicated in diseases3, but for the majority, the cargo and auxiliary lipids facilitating transfer remain unknown. We have combined biochemical, lipidomic and computational methods to systematically characterize LTP-lipid complexes4 and measure how LTP gains of function affect cellular lipidomes. We identified bound lipids for approximately half of the hundred LTPs analyzed, confirming known ligands, while discovering new ones across most LTP families. Gains in LTP function affected the cellular abundance of both their known and newly identified lipid ligands, indicating comparable functional relevance of the two ligand sets. Using structural bioinformatics, we have characterized mechanisms contributing to lipid selectivity, identifying preferences based on head group or acyl chain. We demonstrate some basic principles of how LTPs mobilise their ligands. They commonly interact with several classes of lipids and exhibit broad but selective preference, not only for particular head groups, but also for lipid species with shorter acyl chains containing one or two unsaturations, suggesting that only subsets of lipid species are efficiently mobilized. The datasets represent a resource for further analysis in different cell types and states, such as those associated with pathologies.
    DOI:  https://doi.org/10.1038/s41586-025-10040-y
  5. Curr Opin Clin Nutr Metab Care. 2026 Jan 07.
       PURPOSE OF REVIEW: Cancer cachexia is a complex multiorgan wasting syndrome that negatively impacts on cancer patient's survival and quality of life. Standard nutritional support is considered insufficient to counteract cachexia, and no approved nutritional approach or standard of care for cachexia exists so far. This review highlights recent reports focused on nutrition, aimed at sparing skeletal muscle and targeting molecular pathways underlying cachexia with specific supplements.
    RECENT FINDINGS: In animal models of cancer cachexia, branched-chain amino acids (BCAAs) help restore skeletal muscle proteostasis. In combination with the alanine dipeptide, with strong proteinogenic potential, BCAAs enhance anabolic signaling and suppress proteolysis via mTOR. α-ketoisocaproate exerts additional protective effects against muscle loss by targeting the Akt/FoxO3a and myostatin signaling. Methionine and the derivative SAM improve muscle status via epigenetic control and REDD1 suppression. L-carnitine shows multitarget functions, including muscle proteostasis control, inflammation attenuation, and reduced muscle fibrosis. Omega-3 polyunsaturated fatty acids show anti-inflammatory properties, improve the nutritional status, and prevent adipose tissue browning.
    SUMMARY: Overall, recent findings in preclinical and partly in clinical studies indicate that nutrient-based interventions target complementary cancer cachexia alterations. It is likely that combinatorial approaches, integrating several specific nutrients, will provide an effective base for managing cancer patients during the long journey of the disease, building future interventions against cancer cachexia.
    Keywords:  cancer cachexia; mechanisms; muscle wasting; nutritional support
    DOI:  https://doi.org/10.1097/MCO.0000000000001207
  6. Nat Cancer. 2026 Jan 05.
      Different forms of epithelial-to-mesenchymal transition (EMT) manifest during tumor progression. Little is known about the mechanistic basis and functional role of these distinct EMTs. We explored this question in lung adenocarcinoma (LUAD) primitive progenitors, which are competent to enter dormancy in response to transforming growth factor-β (TGFβ) upon metastatic dissemination. The TGFβ response in these cells includes growth arrest and a full EMT that subsequently transitions into an atypical mesenchymal state of round morphology and lacking actin stress fibers. TGFβ drives this transition by inducing expression of the actin depolymerizing protein gelsolin, which converts a migratory, stress-fiber-rich phenotype into a cortical actin-rich, spheroidal state. This transition lowers the biomechanical stiffness of metastatic progenitors and protects them from killing by cytotoxic lymphocytes. Gelsolin-deficient LUAD progenitors can enter dormancy but succumb to immune surveillance. Thus, quiescent LUAD metastatic progenitors undergo an atypical EMT to avert immune surveillance during TGFβ-driven metastatic dormancy.
    DOI:  https://doi.org/10.1038/s43018-025-01094-y
  7. Trends Cancer. 2026 Jan 02. pii: S2405-8033(25)00311-5. [Epub ahead of print]
      Cancer cells often retain lineage- and tissue of origin-specific programs established prior to malignant transformation. This observation has been elaborated by advances in single-cell and lineage-tracing technologies, which provide high-resolution mapping of these features. Here, we provide an overview of these recent technological developments and examine how the tissue of origin shapes tumor behavior and vulnerabilities. We discuss how the preferential selection of oncogenic drivers by specific tissues leads to distinct genetic alterations across cancers. We then explore the continued dependence of cancer cells on lineage-specific physiological functions and signaling pathways, thereby revealing lineage-dependent therapeutic targets. Finally, we highlight how lineage-specific cell surface marker expression informs precision immunotherapies. Together, these insights are driving a shift toward therapies tailored to the developmental and functional identities of cancer cells.
    Keywords:  cancer specialized function; high-resolution mapping; lineage dependencies; lineage-tracing systems; precision oncology; targeted therapies; tissue-selective oncogenic drivers; tumor antigen repertoire for advanced T cell therapies; tumor tissue of origin
    DOI:  https://doi.org/10.1016/j.trecan.2025.12.004
  8. Commun Biol. 2026 Jan 05. 9(1): 1
      The autophagy receptor p62 is degraded via autophagy under hyperosmotic stress, but whether this involves the formation of biomolecular condensates (p62 bodies) remains unclear. Using human cells, we found that p62 bodies formed within 1 minute of hyperosmotic stress, and increased with stress severity. They formed faster and under milder stress than stress granules, a classic condensate, and exhibited liquid-like properties. Unlike stress granules, p62 bodies frequently colocalized with LC3 and WIPI-2, and were degraded via autophagy. Correlative light and electron microscopy revealed that these p62 bodies were more compact than stress granules and were often associated with the autophagic isolation membrane. Autophagy receptors NBR1 and TAX1BP1, but not OPTN1 or NDP52, behaved similarly to p62, and p62 bodies preferentially contained K63-linked ubiquitin chains. p62 body formation was also observed in human epithelial organoids in association with WIPI-2. Collectively, these results indicate that p62 bodies function as a platform of degradation under hyperosmotic stress.
    DOI:  https://doi.org/10.1038/s42003-025-09190-6
  9. Sci Adv. 2026 Jan 09. 12(2): eadz7607
      Membrane fission is an energy-consuming process, critical for all domains of life. Prototypical fission machineries use local energy input such as nucleoside triphosphate hydrolysis to constrict and cut membranes. However, some membrane fission reactions paradoxically rely on protein scaffolds that by themselves stabilize rather than cut membranes. It turns out these proteins do not work alone; they use nonlocal energy input that generates a membrane tension gradient. Such a gradient mobilizes membrane flow that in turn tends to relax the membrane tension gradient. By interfering with membrane flow, the protein scaffold causes the membrane tension to increase unchecked to the point of mechanical failure, membrane fission. This friction-driven scission (FDS) mechanism is generic, conserved from bacteria to humans, and only requires two ingredients: a membrane tension generating process and a protein scaffold that hinders the associated membrane flow. Because both are often present in cells, it is likely that FDS contributes to membrane fission more frequently than previously appreciated.
    DOI:  https://doi.org/10.1126/sciadv.adz7607
  10. Biophys J. 2026 Jan 06. pii: S0006-3495(26)00005-6. [Epub ahead of print]
      Cytoplasmic proteins must recruit to membranes to function in processes such as endocytosis and cell division. Many of these proteins recognize not only the chemical structure of the membrane lipids, but the curvature of the surface, binding more strongly to more highly curved surfaces, or curvature sorting. Curvature sorting by amphipathic helices is known to vary with membrane bending rigidity, but changes to lipid composition can simultaneously alter membrane thickness, spontaneous curvature, and leaflet symmetry, thus far preventing a systematic characterization of lipid composition on such curvature preferences through either experiment or simulation. Here we develop and apply a bilayer continuum membrane model that can tractably address this gap, quantifying how controlled changes to each material property can favor or disfavor protein curvature sorting. We evaluate both energetic and structural changes to vesicles upon helix insertion, with strong agreement to new in vitro experiments and all-atom MD simulations, respectively. Our membrane model builds on previous work to include both monolayers of the bilayer via representation by continuous triangular meshes. We introduce a coupling energy that captures the incompressibility of the membrane and approximates the established energetics of lipid tilt without using an explicit tilt field. In agreement with experiment, our model predicts stronger curvature sorting in membranes with distinct tail groups (POPC vs DOPC vs DLPC), despite having identical head-group chemistry; the model shows that the primary driving force for weaker curvature sorting in DLPC is that it is thinner, and more wedge shaped. Somewhat surprisingly, asymmetry in lipid shape composition between the two leaflets has a negligible contribution to membrane mechanics following insertion. Our multi-scale approach can be used to quantitatively and efficiently predict how changes to membrane composition in flat to highly curved surfaces alter membrane energetics driven by proteins, a mechanism that helps proteins target membranes at the correct time and place.
    DOI:  https://doi.org/10.1016/j.bpj.2026.01.005
  11. Cell Chem Biol. 2026 Jan 06. pii: S2451-9456(25)00393-9. [Epub ahead of print]
      Ferroptosis is an iron-dependent form of regulated necrosis driven by phospholipid peroxidation. Its suppression relies on a multilayered surveillance system-including neutralizing phospholipid peroxides, terminating the propagation of lipid peroxidation, and limiting the substrates for phospholipid peroxidation-that operates across subcellular compartments and adapts to tissue-specific demands. Rather than functioning redundantly, these defense mechanisms are deployed in a resilient, context-specific manner, shaped by the metabolic profiles, redox states, and regenerative capacities of distinct cell types. Intact ferroptosis surveillance may be especially crucial for post-mitotic cells such as neurons, as its failure can lead to oxidative damage and irreversible degeneration. In contrast, cancer cells actively acquire ferroptosis resistance by upregulating antioxidant networks and reprogramming lipid metabolism, thereby creating a therapeutic vulnerability. Understanding how ferroptosis surveillance is spatially organized and dynamically regulated provides a framework for precision interventions-restoring redox resilience in degenerative disease or selectively inducing ferroptosis in tumors.
    Keywords:  ferroptosis; ferroptosis surveillance; free radical trapping; lipid peroxidation; phospholipid remodeling
    DOI:  https://doi.org/10.1016/j.chembiol.2025.11.013
  12. Anal Chim Acta. 2026 Jan 22. pii: S0003-2670(25)01346-7. [Epub ahead of print]1384 344952
       BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers, mainly due to the late diagnosis and the lack of reliable biomarkers. Lipidomics provides a promising approach for identifying disease-related alterations, but existing methods are often limited to lipid class profiles with insufficient molecular detail. Reversed-phase ultrahigh-performance liquid chromatography coupled to tandem mass spectrometry (RP-UHPLC/MS/MS) offers the possibility to determine lipids at the fatty acyl/alkyl level. Here, we address the need for a validated quantitative workflow that enables accurate and reproducible lipidomic profiling of human serum in the context of PDAC.
    RESULTS: We developed and validated an RP-UHPLC/MS/MS method using multiple reaction monitoring, enabling the identification of 455 lipid species from 22 subclasses, with 381 species from 21 subclasses quantified. The workflow included a response factor correction for sterol esters, which markedly improved their quantification accuracy. The application to serum samples from 54 PDAC patients and 55 healthy controls yielded highly reproducible data, with clear group separation observed in both unsupervised and supervised statistical analyses. Dysregulation was most prominent in sphingolipids and phospholipids. Very long-chain saturated sphingolipids (≥C22) were downregulated, while some shorter or unsaturated chains showed mild upregulation. Phospholipid alterations were dominated by species containing polyunsaturated fatty acyls, particularly 18:2 and 20:4, with plasmalogens showing the strongest changes. These structurally resolved findings were further supported by gas chromatography - mass spectrometry analysis of fatty acid methyl esters.
    SIGNIFICANCE: This validated workflow provides comprehensive quantitative coverage across 21 lipid subclasses with the structural resolution critical for biological interpretation. The detailed mapping of sphingolipid and phospholipid dysregulation in PDAC demonstrates that only the fatty acyl level annotation reveals molecular signatures that may reflect specific enzymatic activities or pathways. The method delivers a robust platform for biomarker discovery and mechanistic studies in cancer lipidomics.
    Keywords:  Human serum; Lipidomics; Mass spectrometry; Pancreatic cancer; Reversed-phase liquid chromatography
    DOI:  https://doi.org/10.1016/j.aca.2025.344952
  13. bioRxiv. 2025 Dec 27. pii: 2025.12.27.696673. [Epub ahead of print]
      Metastasis-the process by which cancer cells spread beyond the primary tumor to distant organs-accounts for the vast majority of cancer-related deaths. To elucidate mechanisms underlying dissemination and metastasis in prostate cancer, we have investigated circulating tumor cells (CTCs) obtained from genetically engineered mouse models (GEMMs). The phenotypic and molecular properties of the CTCs, and organoids derived from these CTCs, closely model the tumor and metastatic phenotypes of their parental GEMMs. Moreover, organoids derived from individual CTCs exhibit molecular and morphological heterogeneity that is associated with distinct metabolic states as well as differences in human prostate cancer outcome. Using computational systems analyses, we have identified TMPO , encoding the nuclear membrane protein lamina-associated polypeptide 2 (Lap2), as a key driver of this heterogeneity. TMPO activity is upregulated in advanced human prostate tumors, metastases, and CTCs, and is associated with adverse clinical outcome. Our findings indicate that TMPO promotes dissemination and metastasis in vivo by enhancing survival in conditions of metabolic stress, and reveal a novel mechanistic link between CTC heterogeneity, stress adaptation, and metastatic potential.
    DOI:  https://doi.org/10.64898/2025.12.27.696673
  14. Cell. 2026 Jan 05. pii: S0092-8674(25)01378-9. [Epub ahead of print]
      Understanding the immunogenic properties of different forms of cell death is critical for rationalized antineoplastic therapeutic development. Here, we identify a regulatory axis that suppresses the immunogenicity of ferroptosis. During ferroptosis, but not apoptosis, cuproptosis, or necroptosis, cancer cells release glutathione peroxidase 4 (GPX4), which binds to zona pellucida glycoprotein 3 (ZP3) on the surface of dendritic cells (DCs), activates the 3',5'-cyclic adenosine monophosphate (cAMP)-protein kinase AMP-activated (PRKA) signaling cascade, inhibits glycolysis, and impairs maturation and activation of DCs, leading to a T cell priming defect. Disrupting the interaction between GPX4 and ZP3 restores DC metabolic activity and enhances antitumor immunity. In preclinical models, blockade of this pathway improves cancer immunosurveillance and potentiates cytotoxic T cell responses when combined with chemotherapy, immunochemotherapy, or radiotherapy. Clinically, high ZP3 expression predicts poor prognosis across multiple solid tumor types, while increased circulating GPX4 levels and ZP3 expression in DCs correlate with resistance to first-line therapies. These findings reveal an immunosuppressive danger signal that limits tumor immunity.
    Keywords:  cancer therapy; cell death; immunogenicity; oxidative stress; zona pellucida family
    DOI:  https://doi.org/10.1016/j.cell.2025.12.002
  15. Nature. 2026 Jan;649(8096): 282-284
      
    Keywords:  Cancer; Cell biology; Diseases; Drug discovery
    DOI:  https://doi.org/10.1038/d41586-025-04149-3
  16. Nat Commun. 2026 Jan 08.
      T-cell avidity is a major determinant of Adoptive T cell therapy (ACT) efficacy for cancer treatment. However, high-avidity tumor-specific T cells can rarely be isolated from cancer patients, highlighting the need for strategies to enhance the cytotoxic capacity of low-avidity cells. Here, we rescue the anti-tumor functions of low-avidity T cells against pancreatic ductal adenocarcinoma (PDAC) by knocking-out TIGIT, a key inhibitory molecule expressed on exhausted CD8+ T cells infiltrating gastrointestinal tumors. We uncover that TIGIT disruption by base editing boosts the intracellular signal transduction derived from a weak T cell receptor (TCR) engagement enforcing cytoskeletal rearrangements, thus increasing T cell avidity and stabilizing the immunological synapse. Accordingly, TIGIT disruption enables low-avidity T cells to exert robust degranulation, comparable to that of high-avidity T cells, and potent and durable anti-tumor capacity in vivo in male mice. These results highlight TIGIT knockout as a potential strategy to enhance low-avidity T cell function and broaden the repertoire of TCR engineered T cells in the treatment of pancreatic cancer and other solid malignancies.
    DOI:  https://doi.org/10.1038/s41467-025-67263-w
  17. bioRxiv. 2025 Dec 31. pii: 2025.12.30.697119. [Epub ahead of print]
      Cell mechanics play significant roles in all aspects of cell function. While many types of fluorescent linear force sensors inserted in cellular fibrillar elements have been developed, few tools are available to track two-dimensional tension in cell membranes. Here, we present a novel principle for tension detection using a fluorescent probe based on the scaffold of the GsMTx4 peptide from Grammostola venom. Previously, we have shown that amphipathic GsMTx4 binds to lipids and inhibits mechanosensitive channels by inserting more deeply into the membrane at tensions near activation thresholds, thereby acting as a buffer clamping lateral pressure in the bilayer. We leverage this property of GsMTx4 to redistribute between the 'shallow' and 'deep' immersion states, thereby designing probes with a fluorescent moiety that increases quantum yield in nonpolar environments. GsMTx4 analogs carrying fluorescent groups at the two positions increase fluorescence intensity in osmotically shocked liposomes and aspirated giant vesicles in a near-linear fashion in response to physiological bilayer tensions. The responses show dependence on membrane composition, particularly lipid charge and the presence of lipid-ordering components, such as sphingomyelin and cholesterol. Langmuir compression isotherms recorded in the presence of NBD analogs indicated initial incorporation into the monolayer, followed by sharp expulsion at the monolayer-bilayer equivalence pressure, with correlated changes in monolayer compressibility and fluorescence, illustrating the basic principle of probe action. The probes show promise for monitoring tension in biological membranes at low, non-inhibitory concentrations. Experiments with native cell-derived membrane vesicles reveal heterogeneous baseline staining and tension responses, underscoring the probes' selectivity for distinct membrane domains.
    Significance: Cell mechanics are crucial for all cell functions, including division, survival, migration, and differentiation. Although many versions of fluorescent linear force sensors have been developed for cytoskeletal and ECM elements, few tools exist to monitor two-dimensional tension in cell membranes. Many cells are motile, actively deforming their membrane, supported and driven by the underlying cytoskeleton. There is a two-order-of-magnitude discrepancy between membrane tension estimates from the tether formation technique and the tensions that activate common mechanosensitive channels in most cells. This discrepancy highlights the need for non-invasive membrane probes that can independently measure membrane tension, especially since it can be highly localized and dynamic. Here, we introduce such probes and a new principle for tension measurement.
    DOI:  https://doi.org/10.64898/2025.12.30.697119
  18. bioRxiv. 2025 Dec 23. pii: 2025.12.20.695739. [Epub ahead of print]
      Senescence and the senescence associated secretory phenotype (SASP) are implicated in promoting early tumorigenesis but due to the complexity of SASP it has been difficult to identify the responsible factors. We used canonical SASP factors on our microenvironment microarray (MEMA) platform to systematically identify SASP-associated drivers of tumorigenesis in breast and lung cancer cells. We found multiple SASP factors enhanced the proliferation and overall cell numbers for both lung and breast cells grown on the MEMA, and that there was significant overlap in SASP-associated growth-promoting factors between the two different cell types. We validated the ability of several factors, including IL-6, TGF-β and EGF, to drive growth in in vitro assays. Interestingly, these factors were effective in driving growth and survival in cells that were altered (either immortalized or fully transformed) but not in normal cells and impacted breast cells differently depending on the age of the patient. RNAseq identified upregulation of wound-healing and stem-cell programs in SASP factor-treated cells. Many of these same SASP factors were present in conditioned media collected from senescent cells, which enhanced the growth of both lung and breast cancer cells, and inhibitors of the specific SASP factors partially reduced growth. Similarly, targeted inhibition of EGF partially reduced lung tumour growth in xenografts when senescent but not normal fibroblasts were co-implanted. Our findings have identified core SASP drivers of tumorigenesis and suggest that effective tumorigenesis driven by SASP is multifactorial and requires alterations in the target cells to achieve maximal response.
    Keywords:  Antitumor Assays; Breast Cancer; Lung Cancer; Microenvironment Microarray; Senescence; Senescence-Associated Secretory Phenotype; Tumour Microenvironment; Xenograft Model
    DOI:  https://doi.org/10.64898/2025.12.20.695739
  19. bioRxiv. 2025 Dec 23. pii: 2025.12.21.695848. [Epub ahead of print]
      Ferroptosis is an iron-catalyzed lipid peroxidation (LP)-dependent cell death. Induction of mitochondrial ROS (mtROS) is crucial in the execution of ferroptosis, but the underlying mechanism remains unclear. Through utilizing the hepatocyte model and RNA-seq analysis, we determined mtROS-dependent metabolic changes that modulate ferroptosis sensitivity. Elevated mtROS production and LP suppressed glycolysis, fatty acid oxidation, and citric acid cycle activity, representing adaptive responses that protect cells from ferroptosis. On the other hand, mtROS-driven signaling impaired glutathione biosynthesis and downregulated genes involved in coenzyme Q10 (CoQ) biosynthesis, including those in the mevalonate pathway and CoQ8A, a key stabilizer of the CoQ biosynthetic complex. Importantly, silencing CoQ8A expression enhanced, whereas overexpression of CoQ8A reduced, ferroptosis susceptibility of hepatocytes and various cancer cell types. The mtROS-mediated downregulation of CoQ8A was dependent on farnesoid X receptor (FXR) and retinoid X receptors (RXRs). Collectively, our findings highlight that mtROS promotes ferroptosis, at least in part, by suppressing glutathione and CoQ biosynthesis.
    DOI:  https://doi.org/10.64898/2025.12.21.695848
  20. EMBO J. 2026 Jan 06.
      The rapid, transient, and unpredictable nature of interactions between circulating cells and the endothelium challenges the investigation of these events under flow conditions. Here, we developed an imaging and image-analysis framework called FlowVision, which integrates fast, bright-field live-cell imaging with deep-learning-based image analysis to quantitatively track cell landing and arrest on an endothelial monolayer under physiological flow conditions. Using FlowVision, we find that pancreatic ductal adenocarcinoma (PDAC) cells exhibit variable adhesion strength and flow sensitivity. Remarkably, some PDAC cells demonstrate comparable endothelial engagement to leukocytes, preferentially arresting at endothelial junctions, providing them access to the underlying basal extracellular matrix. PDAC cells attach and form clusters in areas with high expression of the endothelial CD44 receptor. Targeting CD44 using siRNA, function-blocking antibodies, or degrading its ligand, hyaluronic acid (HA), strongly reduces PDAC cell attachment. Overall, our label-free live-imaging approach demonstrates that cancer and immune cells share both common and unique features in endothelial adhesion under flow, and allows identification of CD44 and HA as key mediators of PDAC cell arrest.
    Keywords:  Adhesion; Circulating Immune Cells; Circulating Tumor Cells; Deep Learning; Image Analysis
    DOI:  https://doi.org/10.1038/s44318-025-00678-9
  21. Mol Cell. 2026 Jan 08. pii: S1097-2765(25)00980-3. [Epub ahead of print]86(1): 135-149.e9
      Mitochondria and the endoplasmic reticulum (ER) contain large areas that are in close proximity. Yet the mechanism of how these inter-organellar adhesions are formed remains elusive. Tight functional connections, termed "membrane contact sites," assemble at these areas and are essential for exchanging metabolites and lipids between the organelles. Recently, the ER-resident protein PDZ domain-containing protein 8 (PDZD8) was identified as a tether between the ER and mitochondria or late endosomes/lysosomes. Here, we show that PDZD8 can undergo phase separation via its intrinsically disordered region (IDR). Endogenously labeled PDZD8 forms condensates on membranes both in vitro and in mammalian cells. Electron microscopy analyses indicate that the expression of full-length PDZD8 rescues the decrease in inter-organelle contacts in PDZD8 knockout cells but not PDZD8 lacking its IDR. Together, this study identifies that PDZD8 condensates at the lipid interfaces act as an adhesive framework that stitches together the neighboring organelles and supports the structural and functional integrity of inter-organelle communication.
    Keywords:  PDZD8; biomolecular condensates; endoplasmic reticulum; liquid-liquid phase separation; membrane contact sites; mitochondria
    DOI:  https://doi.org/10.1016/j.molcel.2025.12.006
  22. EMBO J. 2026 Jan 03.
      After damage from pathogenic, chemical or physical stress, endolysosomal membranes are repaired and resealed by the endosomal sorting complex required for transport (ESCRT) machinery, but how this membrane damage is sensed and translated into ESCRT recruitment is poorly understood. Here, we identify the two ATG8 E3-like ligases, ATG16L1 and TECPR1, as ion-dependent catalysts for ESCRT recruitment to damaged lysosomal membranes. Leakage from perforated lysosomes induces the proton sensitive V-ATPase-dependent recruitment of ATG16L1-ATG5-ATG12 complexes, or the calcium-sensitive sphingomyelin-dependent recruitment of TECPR1-ATG5-ATG12 complexes. In both cases, the E3-like complex-dependent ATG5-ATG12 conjugate is required for ESCRT recruitment to the damaged membrane, and stabilization of the ESCRT machinery. Collectively, this study establishes the ATG8 E3-like ligases as membrane damage sensors for ESCRT-mediated membrane repair.
    Keywords:  ATG8 E3-like Ligases; CASM; ESCRT; Lysosomal Membrane Integrity; Membrane Damage Sensor
    DOI:  https://doi.org/10.1038/s44318-025-00672-1
  23. Science. 2026 Jan 08. eady5532
      Environmental adaptation often involves a shift in energy utilization toward mitochondrial fatty acid oxidation, which requires carnitine. Besides dietary sources of animal origin, carnitine biosynthesis from trimethyllysine (TML) is essential, particularly for those who consume plant-based diets; however, its molecular regulation and physiological role remain elusive. Here, we identify SLC25A45 as a mitochondrial TML carrier that controls carnitine biosynthesis and fuel switching. SLC25A45 deficiency decreased the carnitine pool and impaired mitochondrial fatty acid oxidation, shifting reliance to carbohydrate metabolism. Slc25a45-deficient mice were cold-intolerant and resistant to lipid mobilization by GLP1 receptor agonist (GLP-1RA), rendering them resistant to adipose tissue loss. Our study suggests that mitochondria serve as a regulatory checkpoint in fuel switching, with implications for metabolic adaptation and the efficacy of GLP-1RA-based anti-obesity therapy.
    DOI:  https://doi.org/10.1126/science.ady5532
  24. Nat Commun. 2026 Jan 03.
      Colorectal cancer (CRC) frequently develops aggressive metastatic disease, yet the cellular features that enable dissemination remain poorly defined. IKKα, a kinase traditionally linked to stress and inflammatory signaling, is increasingly recognized for broader functions in cancer. Here, we show that loss of IKKα unexpectedly promotes metastasis in CRC. Using patient-derived organoids, we find that genetic or pharmacological inhibition of IKKα stabilizes tight-junction components, leading to the emergence of compact epithelial clusters with a heightened ability to spread and colonize the liver. Single-cell transcriptomics reveals expansion of a CDH17⁺/CLDN2⁺ epithelial subpopulation that dominates metastatic lesions, a finding validated by tissue staining. Remarkably, disrupting CLDN2 completely eliminates the metastatic advantage caused by IKKα loss. These results identify a metastasis-competent epithelial state driven by tight-junction remodeling and uncover a vulnerable node that may be exploited therapeutically in aggressive colorectal cancer.
    DOI:  https://doi.org/10.1038/s41467-025-68169-3
  25. bioRxiv. 2026 Jan 02. pii: 2025.12.31.697247. [Epub ahead of print]
      Quantitative, time-resolved 3D fluorescence microscopy can reveal complex cellular dynamics in living cells and tissues. Broader use remains limited by the difficulty of identifying, segmenting, and tracking objects of different size and shape in crowded intracellular environments in low-contrast, anisotropic, monochromatic image volumes. Objects overlap, deform, appear and disappear, and span wide ranges of size and intensity. Classical segmentation pipelines typically require high signal-to-noise data and rely on intensity heuristics with hand-tuned postprocessing that generalize poorly. Supervised deep learning methods require extensive voxel-level annotations that are costly, inconsistent across phenotypes, and rapidly become obsolete as imaging conditions change. We introduce SpatialDINO, a fully automated self-supervised method that trains a native 3D vision transformer, based on a modified version of DINOv2(1). SpatialDINO yields robust semantic feature maps from single channels of multi-channel microscopy that, irrespective of object shape, support object detection and segmentation directly from naïve 3D images across z-spacings and numbers of planes and different imaging modalities, without retraining or voxel annotations. We trained SpatialDINO on a small set of confocal volumes acquired by live-cell fluorescent 3D lattice light-sheet microscopy, spanning targets of different size and shape located in crowded cellular environments, from diffraction-limited clathrin coated pits and clathrin coated vesicles to bigger structures including endosomes and lysosomes, and endosomes and lysosomes pharmacologically enlarged to highlight endosomal membrane profiles. Post-processing of the features generated by SpatialDINO allows detection and unique object identification of these objects in naïve 3D images. It also enables detection of significantly different previously unseen object classes, such as cellular plasma membranes and nuclei and even tumors in MRI scans. Finally, we illustrate its value by tracking endosomes in 3D time series, combining SpatialDINO-derived feature similarity with spatial proximity to improve association through occlusion, abrupt appearance changes, and dense packing - all conditions that have been challenging for existing methods. SpatialDINO therefore lowers a major barrier to quantitative analysis of heterogeneous, monochromatic objects in crowded 3D cellular environments.
    SUMMARY: Lavaee et al. have developed SpatialDINO to surmount the difficulties presented by attempting to identify, segment, and track objects in crowded volumes. SpatialDINO is a self-supervised, native 3D vision transformer trained directly on unlabeled fluorescence volumes acquired by live-cell 3D lattice light-sheet microscopy. By learning dense volumetric representations without voxel-level supervision, SpatialDINO generates features that enable fully automated detection, segmentation, and tracking of subcellular structures across a wide range of sizes and morphologies in crowded, anisotropic 3D/4D datasets acquired with different microscopy modalities. The approach generalizes across targets and imaging conditions without further training, reducing dependence on manual annotation while maintaining performance in complex cellular environments.
    SIGNIFICANCE: SpatialDINO brings a self-supervised foundation model for analyzing 3D fluorescence microscopy images by adapting DINOv2-style joint-embedding training to learn dense volumetric features directly from unlabeled 3D datasets. By exploiting true 3D context rather than slice-wise "2.5D" aggregation, it enables automated detection and segmentation in crowded, anisotropic, low-contrast volume and enables tracking in 4D time-lapse data. SpatialDINO generalizes across targets and imaging conditions without voxel-level annotation or retraining.
    DOI:  https://doi.org/10.64898/2025.12.31.697247
  26. EMBO Rep. 2026 Jan 05.
      Effective visualization of 3D microscopy data is essential for communicating biological results. While scientific 3D rendering software is specifically designed for this purpose, it often lacks the flexibility found in non-scientific software like Blender, which is a free and open-source 3D graphics platform. However, loading microscopy data in Blender is not trivial. To bridge this gap, we introduce Microscopy Nodes, an extension for Blender that enables the seamless integration of large microscopy data. Microscopy Nodes provides efficient loading and visualization of up to 5D microscopy data from Tif and OME-Zarr files. Microscopy Nodes supports various visualization modes including volumetric, isosurface, and label-mask representations, and offers additional tools for slicing, annotation, and dynamic adjustments. By leveraging Blender's advanced rendering capabilities, users can create high-quality visualizations that accommodate both light and electron microscopy. Microscopy Nodes makes powerful, clear data visualization available to all researchers, regardless of their computational experience, and is available through the Blender extensions platform with comprehensive tutorials.
    Keywords:  3D Data; Blender; Data Visualization; Electron Microscopy; Fluorescence Microscopy
    DOI:  https://doi.org/10.1038/s44319-025-00654-8
  27. Angew Chem Int Ed Engl. 2026 Jan 08. e19056
      The plasma membrane exhibits diverse substructures, such as pseudopodia, membrane nanotubes, and migrasomes, that are essential for cellular communication and cargo transport. Imaging these fine structures remains challenging due to their nanoscale dimensions and limitations of existing fluorescent probes. Here, we report the development of two rhodamine-based probes, RSD1 and RSD2, incorporating anionic membrane-anchoring groups and pyrrolidine auxochromes to enable wash-free, serum-compatible, long-term plasma membrane imaging. RSD2, in particular, demonstrates superior fluorogenicity, brightness, and photoswitching properties, facilitating high-resolution imaging in both live and fixed cells. It selectively labels membrane substructures across diverse cell types and maintains membrane specificity in the presence of serum. RSD2 is compatible with advanced microscopy techniques including confocal microscopy, instant structured illumination microscopy (iSIM), and direct stochastic optical reconstruction microscopy (dSTORM), achieving up to 40 nm resolution. Using two-color dSTORM, we visualize silica nanoparticle trafficking via membrane nanotubes and gondola-like bulges in neuronal cells, marking the first such observation. RSD2 also enables imaging of migrasomes and retraction fibers, revealing dynamic membrane-mediated transport processes. This probe offers a robust and versatile platform for investigating membrane architecture and function, with broad applicability in cell biology, nanomedicine, and super-resolution imaging.
    Keywords:  Fluorescent probe; Imaging; Plasma membrane; Rhodamine; Super‐resolution
    DOI:  https://doi.org/10.1002/anie.202519056
  28. Autophagy. 2026 Jan 04. 1-18
      Lysosome homeostasis is vital for cellular fitness due to the essential roles of this organelle in various pathways. Given their extensive workload, lysosomes are prone to damage, which can stimulate lysosomal quality control mechanisms such as biogenesis, repair, or autophagic removal - a process termed lysophagy. Despite recent advances highlighting lysophagy as a critical mechanism for lysosome maintenance, the extent of lysosome integrity perturbation and the magnitude of lysophagy in vivo remain largely unexplored. Additionally, the pathophysiological relevance of lysophagy is poorly understood. To address these gaps, it is necessary to develop quantifiable methods for evaluating lysosome damage and lysophagy flux in vivo. To this end, we created two transgenic mouse lines expressing a tandem fluorescent LGALS3/galectin 3 probe (tfGAL3), either constitutively or conditionally under Cre recombinase control, utilizing the property of LGALS3 to recognize damaged lysosomes. This tool enables spatiotemporal visualization of lysosome damage and lysophagy activity at single-cell resolution in vivo. Systemic analysis across various organs, tissues, and primary cultures from these lysophagy reporter mice revealed significant variations in basal lysophagy, both in vivo and in vitro. Additionally, this study identified substantial changes in lysosome integrity and lysophagy flux in different tissues under stress conditions such as starvation, acute kidney injury and diabetic modeling. In conclusion, these complementary lysophagy reporter models are valuable resources for both basic and translational research.Abbreviation: AAV: adeno-associated virus; ATG7: autophagy related 7; CA-tfGAL3: cre-recombinase-activated tandem fluorescent LGALS3; DAPI: 4',6-diamidino-2-phenylindole; DM: diabetes mellitus; ESCRT: endosomal sorting complex required for transport; GFP: green fluorescent protein; HFD: high-fat diet; Igs2/H11/Hipp11: intergenic site 2; IST1: IST1 factor associated with ESCRT-III; KI: knock-in; LAMP1: lysosomal-associated membrane protein 1; LGALS3: lectin, galactoside-binding, soluble, 3; LLOMe: L-leucyl-L-leucine methyl ester hydrobromide; MEFs: mouse embryonic fibroblasts; NaOx: sodium oxalate; PDCD6IP: programmed cell death 6 interacting protein; PTECs: proximal tubular epithelial cells; RFP: red fluorescent protein; STZ: streptozotocin; TAM: tamoxifen; tfGAL3: tandem fluorescent LGALS3; TMEM192: transmembrane protein 192.
    Keywords:  In vivo; lysophagy; lysosome; lysosome damage; ratiometric probe
    DOI:  https://doi.org/10.1080/15548627.2025.2608974
  29. bioRxiv. 2026 Jan 02. pii: 2026.01.01.697161. [Epub ahead of print]
      Despite advances in fluorescence microscopy, spectral overlap and limited resolution hinder the dense mapping of the cellular ultrastructure. To overcome these challenges, we developed Cy-ExM, a high-plex imaging strategy that integrates optimized cryo-fixation for antigen preservation, expansion microscopy, and iterative immunofluorescence labeling. Using oblique plane microscopy, we perform three-dimensional super-resolution imaging of 20 biological targets encompassing the full cellular volume of individual mammalian cells.
    DOI:  https://doi.org/10.64898/2026.01.01.697161
  30. Eur Phys J E Soft Matter. 2026 Jan 08. 49(1-2): 2
      Cells within biological tissue are constantly subjected to dynamic mechanical forces. Measuring the internal stress of tissues has proven crucial for our understanding of the role of mechanical forces in fundamental biological processes like morphogenesis, collective migration, cell division or cell elimination and death. Previously, we have introduced Bayesian inversion stress microscopy (BISM), which is relying on measuring cell-generated traction forces in vitro and has proven particularly useful to measure absolute stresses in confined cell monolayers. We further demonstrate the applicability and robustness of BISM across various experimental settings with different boundary conditions, ranging from confined tissues of arbitrary shape to monolayers composed of different cell types. Importantly, BISM does not require assumptions on cell rheology. Therefore, it can be applied to complex heterogeneous tissues consisting of different cell types, as long as they can be grown on a flat substrate. Finally, we compare BISM to other common stress measurement techniques using a coherent experimental setup, followed by a discussion on its limitations and further perspectives.
    DOI:  https://doi.org/10.1140/epje/s10189-025-00542-y
  31. Mol Cell. 2026 Jan 08. pii: S1097-2765(25)00985-2. [Epub ahead of print]86(1): 3-5
      In this issue of Molecular Cell, Kral et al.1 identify a targetable, novel mechanism of pancreatic ductal adenocarcinoma (PDAC) tumorigenesis via SRSF1 splicing-mediated regulation of an Alu-derived exon in Aurora kinase A (AURKA).
    DOI:  https://doi.org/10.1016/j.molcel.2025.12.011
  32. Cell. 2026 Jan 08. pii: S0092-8674(25)01423-0. [Epub ahead of print]189(1): 3-5
      Heme carries oxygen and is critical for the control of redox reactions. In this issue of Cell, Lewis and Gruber et al. demonstrate how low concentrations of heme destabilize complex IV of the respiratory chain to release copper and kill acute myeloid leukemia cells by cuproptosis.
    DOI:  https://doi.org/10.1016/j.cell.2025.12.010
  33. J Clin Invest. 2026 Jan 06. pii: e193758. [Epub ahead of print]
      Vessels encapsulating tumor clusters (VETC), a distinct vascular pattern in hepatocellular carcinoma (HCC), facilitates non-invasive metastasis in whole cluster. The interaction between VETC and tumor microenvironment requires exploration. Here, we found that compared to human Non-VETC-HCCs, VETC-tumors exhibited more PD1+CD8+ T cells and Tregs, especially TNFRSF4+Tregs and Ki67+Tregs which showed increased immunosuppressive and proliferative activity. Such immunosuppressive status was also detected in tumor emboli of VETC-HCCs, and Treg density in emboli was positively associated with metastatic cell proliferation. VETC-HCCs revealed abundance correlation, closer spatial proximity, and stronger immunosuppressive ligand-receptor interactions between TNFRSF4+Tregs/Ki67+Tregs and PD1+CD8+ T cells. Depleting Tregs in mice reduced PD1+CD8+ T cells in primary lesions, tumor emboli and metastatic foci of VETC-allografts, and attenuated allograft metastasis. TGF-β1 levels were upregulated in endothelial cells of VETC-HCCs and associated with TNFRSF4+Tregs/Ki67+Tregs enrichment. Disrupting VETC formation decreased endothelial TGF-β1 expression, and reduced TNFRSF4+Tregs/Ki67+Tregs, PD1+CD8+ T cells, Treg/CD8+ T cells ratio. Collectively, VETC may enhance Tregs' activity via TGF-β1, while Tregs promote and sustain CD8+ T cell exhaustion through immune inhibitory ligand-receptor interaction, thereby shaping immunosuppressive microenvironment and enabling tumor cluster to carry such niche to disseminate. These findings disclose mechanisms of tumor immune microenvironment formation and provide rationales for precision medicine.
    Keywords:  Hepatology; Immunology; Liver cancer; Tregs; Vascular biology
    DOI:  https://doi.org/10.1172/JCI193758
  34. Biosens Bioelectron. 2026 Jan 06. pii: S0956-5663(26)00009-6. [Epub ahead of print]297 118377
      Evaluating cellular susceptibility to ferroptosis, a regulated cell death process driven by the lipid peroxidation (LPO), is critical for understanding relevant pathogenesis and developing targeted therapies. This objective may be achieved by monitoring LPO within endoplasmic reticulum (ER), which is the earliest site of lipid peroxide accumulation during ferroptosis; however, tools for real-time and in situ detection of LPO in ER remain lacking. Herein, we report an ER-targeting fluorescence probe ER-LPO for monitoring LPO in ER and evaluating ferroptosis susceptibility. ER-LPO exhibited a sensitive, selective and rapid fluorescence off-on response at 518 nm to lipid peroxides, and could monitor both lipoxygenase-catalyzed enzymatic and hydroxyl radical-triggered non-enzymatic LPO. Using ER-LPO imaging, dynamic accumulation of lipid peroxides on the ER membrane was monitored during ferroptosis, which was negatively correlated with cell viability but independent of the induction pathways and cell lines. Notably, increasing polyunsaturated fatty acids (PUFA) in membrane phospholipids through PUFA supplementation or enhancing ACSL4-catalyzed PUFA assimilation accelerated LPO process and heightened cellular susceptibility to ferroptosis. Conversely, supplementing monounsaturated fatty acids or inhibiting ACSL4 to block the PUFA uptake could reduce LPO levels and facilitate ferroptosis resistance of cells. Moreover, ER-LPO enabled high-throughput screening of anti-ferroptosis reagents, identifying baicalein (a trihydroxyflavone derivative) as a potent ferroptosis inhibitor, which may be attributed to its intrinsic antioxidant capacity and lipoxygenase inhibitory activity. As an efficient tool for assessing ferroptosis susceptibility by monitoring of LPO in ER, ER-LPO may offer broad applications in mechanism studies, therapeutic evaluations and new drug developments for ferroptosis-related diseases.
    Keywords:  Endoplasmic reticulum; Ferroptosis susceptibility; Fluorescence probe; High-throughput screening; Lipid peroxidation
    DOI:  https://doi.org/10.1016/j.bios.2026.118377