bims-medica Biomed News
on Metabolism and diet in cancer
Issue of 2026–03–08
eleven papers selected by
Brett Chrest, Wake Forest University



  1. Nat Commun. 2026 Mar 05.
      Respiratory complex I is a multi-subunit energy-transducing membrane enzyme essential for mitochondrial and cellular energy metabolism. It couples NADH oxidation and ubiquinone-10 (Q10) reduction to the concomitant pumping of four protons to generate the proton-motive force that powers oxidative phosphorylation. Despite recent advances in structural knowledge of complex I, many mechanistic aspects including the reactive binding poses of Q10, how Q10 reduction initiates the proton transfer cascade, and how protons move through the membrane domain, remain unclear. Here, we use electron cryomicroscopy to determine structures of mammalian complex I, reconstituted into phospholipid nanodiscs containing exogenous Q10 and reduced by NADH, to global resolutions of 2.0 to 2.6 Å. Two conformations of a reduced Q10H2 molecule are observed, fully inserted into the Q-binding channel in the turnover-relevant closed state. By comparing the quinone species bound in oxidised and reduced complex I structures, paired with molecular dynamics simulations to investigate the charge states of key surrounding residues, we propose a series of substrate binding poses that Q10 transits through for reduction. Our highly hydrated structures exhibit near-continuous proton-transfer connections along the length of the membrane domain, enabling comparisons between them to assist in identifying the proton-transfer control points that are essential to catalysis.
    DOI:  https://doi.org/10.1038/s41467-026-70030-0
  2. Cell. 2026 Feb 27. pii: S0092-8674(26)00115-7. [Epub ahead of print]
      The tricarboxylic acid (TCA) cycle couples nutrient oxidation with the generation of reducing equivalents that power oxidative phosphorylation. Nevertheless, the requirement for components of the TCA cycle is context-specific, raising the question of which TCA cycle outputs support cell fitness. Here, we demonstrate that citrate clearance is an essential function of the TCA cycle. As citrate production increases, so do TCA cycle activity and dependence upon aconitase 2 (ACO2), the enzyme that initiates citrate catabolism in the TCA cycle. Disrupting citrate catabolism activates the integrated stress response and impairs cell fitness, and these effects are reversed by preventing citrate production or promoting mitochondrial citrate efflux. In vivo, ACO2 deficiency induces citrate accumulation and triggers tubular degeneration in the kidney, a tissue that physiologically takes up circulating citrate. Thus, intracellular citrate accumulation can be a metabolic liability, and citrate clearance is a major function of ACO2 in the TCA cycle.
    Keywords:  ACO2; TCA cycle; cell metabolism; citrate; integrated stress response
    DOI:  https://doi.org/10.1016/j.cell.2026.01.028
  3. Mol Metab. 2026 Feb 26. pii: S2212-8778(26)00026-8. [Epub ahead of print] 102342
       PURPOSE OF THE RESEARCH: To develop a sensitive, versatile analytical method capable of simultaneously detecting epigenetically relevant metabolites without chemical derivatization. We also aim to establish a stable isotope tracing methodology to track the biosynthesis of key epigenetic donors, S-adenosylmethionine (SAM) and acetyl-coenzyme A (acetyl-CoA), and demonstrate the method's reproducibility and quantitative accuracy through case-control studies that link metabolism to epigenetics.
    BASIC PROCEDURES: After a comprehensive literature review, we selected 42 metabolites based on their roles in epigenetic processes such as methylation and acetylation, and devised a targeted metabolomics approach to extract, detect, and quantify these metabolites (Supplementary table 1 and Figure 1). We then optimized ionization parameters and scan rate using pure standards to maximize metabolite coverage in LC-MS/MS. We chose a biphasic extraction method adapted from Lotti et al., using phosphoric acid (15%) and methyl tert-butyl ether (MTBE) for efficient extraction of a wide range of metabolites, including short-chain fatty acids (SCFAs) and formate, without the need for chemical derivatization. The organic phase was analyzed by GC-MS/MS, while the aqueous phase was subjected to LC-MS/MS using a zwitterionic HILIC column with medronic acid to improve peak shape and retention of charged metabolites. To potentially link metabolism and epigenetic modifications, we implemented a stable isotope tracing methodology to track 13C-labeled glucose, glutamine, or serine into SAM and acetyl-CoA. Our method focuses on measuring isotopomers rather than isotopologues, offering a nuanced understanding of labeled carbon atom fate.
    MAIN FINDINGS: Our method demonstrated high reproducibility and sensitivity, enabling the quantitative analysis of over 30 epigenetically relevant metabolites, including SCFAs, SAM, and acetyl-CoA, in various biological samples. We successfully quantified these metabolites in three case-control studies: (1) liver and gut content from germ-free and conventional mice, revealing significant differences in SCFA levels and other metabolites linked to one-carbon metabolism and energy production. (2) During OSKM reprogramming of mouse embryonic fibroblasts vitamin B12 supplementation enhances cellular reprogramming. Using 13C-serine as a tracer, we observed a time-dependent increase in SAM enrichment, with additive effects from vitamin B12, primarily due to heightened labeling of the +1 isotopomers formate and methyl group. (3) In an isogenic human glioma cell line with the IDH1 R132H mutation, both wild-type and mutant cells predominantly used glucose carbons for acetyl-CoA synthesis. However, while no significant differences were observed in glucose metabolism between WT and mutant cells, we noted increased glutamine consumption in IDH1-R132H cells, evidenced by higher enrichment of the acetyl group in acetyl-CoA.
    NEW AND IMPORTANT ASPECTS OF OUR STUDY: We present an innovative analytical methodology for the simultaneous detection and quantification of over 30 epigenetically relevant metabolites, including short chain fatty acids. Using stable isotope tracing to track the synthesis of S-adenosylmethionine (SAM) and acetyl-Coenzyme A (acetyl-CoA), our method reveals new insights into metabolism linked to epigenetic modifications, including glycolysis, the pentose phosphate pathway, de novo glycine synthesis, and the folate and methionine cycle. Demonstrating practical utility in case-control studies, this approach supports integrative multi-omics strategies to explore the interplay between metabolism and epigenetics across various biological systems and diseases.
    Keywords:  Epigenetics; Mass spectrometry; Metabolism; Metabolomics; Microbiota; Stable isotope labeling
    DOI:  https://doi.org/10.1016/j.molmet.2026.102342
  4. ACS Chem Biol. 2026 Mar 04.
      Hepatic fructose utilization depends on ketohexokinase mediated phosphorylation to generate fructose-1-phosphate and commit fructose carbons to additional metabolic steps. Since dysregulated fructose metabolism has been directly connected to the onset and progression of liver disease and cancer, there is considerable interest in identifying the contributions of fructose carbons in bioenergetic pathways. An essential technology for assessing fructose utilization has been the application of isotopically labeled fructose and magnetic resonance with the development of 13C hyperpolarized imaging with [2-13C]fructose allowing for in vivo assessments. While hyperpolarized imaging of [2-13C]fructose has achieved remarkable success in the detection of cancer metabolism, this approach has yet to be utilized to assess fed and fasted states in healthy livers. By challenging mice with a 6 h fast, we demonstrate that hyperpolarized [U-2H, 2-13C]fructose in vivo spectroscopy can clearly distinguish direct hepatic gluconeogenesis. Comprehensively, this work aims to establish a foundational methodology for the assessment of hepatic metabolism in vivo.
    DOI:  https://doi.org/10.1021/acschembio.5c00980
  5. Life Sci Alliance. 2026 May;pii: e202503602. [Epub ahead of print]9(5):
      Mitochondria orchestrate energy conversion and cell fate, yet label-free approaches that report both functional and physical states at the single-organelle level are nonexistent. Here, we combine atomic force microscopy (AFM) imaging with single-mitochondrion phenotyping by quantifying stiffness, height, and spontaneous low-frequency height fluctuations at the nanoscale. Across respiratory activators, inhibitors, and uncouplers, the integrated 0- to 20-Hz fluctuation power correlates with mitochondrial membrane potential (ΔΨm) and does not covary with changes in mitochondrial height (a proxy for swelling). In liver mitochondria lacking mitochondrial carrier homolog 2 (MTCH2), a regulator of mitochondrial metabolism, dynamics, and apoptosis, AFM reveals a compact, mechanically stiff, high-fluctuation state consistent with hyperpolarization and distinct from inhibited/uncoupled signatures. Extending the assay to mitochondria isolated from mouse embryonic fibroblasts, AFM data can distinguish between genotypes: loss of the mitochondrial pro-fusion proteins mitofusin 1 or 2 (MFN1 or MFN2) yields stiff, low-fluctuation mitochondria with reduced ΔΨm, whereas MTCH2 loss produces stiff, high-fluctuation, high-ΔΨm mitochondria. These three label-free features provide reproducible single-organelle "fingerprints" that resolve bioenergetic states and molecular defects and complement fluorescence and respirometry.
    DOI:  https://doi.org/10.26508/lsa.202503602
  6. Mol Metab. 2026 Mar 03. pii: S2212-8778(26)00028-1. [Epub ahead of print] 102344
      In natural settings, energy storage and mobilization maintain a dynamic balance in response to recurrent overfeeding and fasting. Imbalanced energy storage and mobilization lead to a variety of metabolic dysfunctions. However, whether the metabolic status directly couples with epigenetic modifications and transcriptional outputs remains unclear. Here, we aimed to investigate the epigenetic mechanism underlying this adaptive balance and observed that, in an overfeeding state, increased glucose availability is associated with enhanced histone acetylation coinciding with acetyl-CoA production in an acyl-CoA short-chain synthetase 2 (ACSS2)-dependent manner, contributing to energy storage (e.g., lipogenesis); in contrast, in the fasting state, elevated D-β-hydroxybutyrate levels are associated with altered histone acetylation distribution and transcriptional programs, supporting a metabolic shift from anabolism to catabolism, such as fatty acid oxidation. In both overfeeding and fasting states, acetylated lysines in the histone require BRD4 to recognize and initiate transcriptional regulation. Inhibition of BRD4 leads to context-dependent phenotypic effects: it ameliorates non-alcoholic fatty liver disease (NAFLD) pathology induced by a high-fat diet, while it exacerbates hepatic steatosis in fasted mice or mice fed a ketogenic diet. Thus, these findings highlights that epigenetic regulation of energy storage and mobilization is closely linked to the availability of glucose, and ketone bodies. Moreover, our study revealed that modulation of ACSS2-associated pathway may represent a potential strategy for treatment of metabolic diseases, such as NAFLD.
    Keywords:  ACSS2; BRD4; Fatty acid oxidation; Histone acetylation; lipogenesis
    DOI:  https://doi.org/10.1016/j.molmet.2026.102344
  7. Methods Enzymol. 2026 ;pii: S0076-6879(26)00025-X. [Epub ahead of print]727 123-143
      Cells continuously metabolize lipids, converting them into diverse molecules that influence cellular functions- in health and disease. Sphingolipids have been specifically linked to a wide range of - cellular processes and have been shown to play a crucial role in the onset and progression of various diseases. Here, we detail a method for measuring lipid flux through a combination of labeled lipids and thin-layer chromatography (TLC). This method describes the exogenous addition of radioactive and fluorescent lipid analogues and the subsequent tracing of their metabolism. This metabolic tracing allows for conclusions to be drawn about the fate of a lipid in a given system. Though the described method focuses on sphingolipids, many alternatives are discussed for adaptation of the method to measurement of any specific lipid of interest. Overall, this method offers a robust, easy-to-adapt approach for measuring lipid flux across different cell types and experimental systems.
    Keywords:  Lipid labeling; Metabolism; Pulse-chase; Sphingolipids; Thin-layer chromatography
    DOI:  https://doi.org/10.1016/bs.mie.2026.01.017
  8. EJHaem. 2026 Apr;7(2): e70253
       Background: Venetoclax plus azacitidine (V+A) is standard for older, intensive-ineligible patients with acute myeloid leukemia (AML). Its expanding use in younger, curative-eligible adults lacks comparative evidence against conventional 7+3 induction, raising uncertainty about potential survival compromise.
    Methods: We performed an age-stratified, retrospective comparative effectiveness study using de-identified TriNetX electronic health records (2018-2025). Adults receiving first-line V+A or 7+3 were propensity-matched 1:1 within prespecified age groups (18-59; ≥60) by demographics, comorbidities, socioeconomic factors, and performance status. The primary endpoint was 1-year all-cause mortality; secondary endpoints included complete remission and ICU admission.
    Results: After matching, 214 younger and 1724 older adults per arm were analyzed. Among younger adults, V+A was associated with significantly higher 1-year mortality versus 7+3 (20.6% vs. 8.9%; HR 2.55), with a number needed to harm of nine. Remission rates favored intensive induction (53.3% vs. 44.9%), while ICU use was similar. In older adults, mortality differences were smaller (23.1% vs. 20.5%; HR 1.34; NNH 38), though remission again favored 7+3.
    Conclusion: V+A appears markedly inferior to 7+3 as first-line therapy in younger, curative-eligible AML, producing a nearly fourfold greater harm signal than in older adults. These findings support restricting V+A to intensive-ineligible patients pending randomized confirmation.
    Trial Registration: The authors have confirmed clinical trial registration is not needed for this submission.
    Keywords:  acute myeloid leukemia; azacitidine; induction chemotherapy; propensity score matching; real‐world evidence; survival outcomes; venetoclax
    DOI:  https://doi.org/10.1002/jha2.70253
  9. iScience. 2026 Mar 20. 29(3): 114954
      Precision oncology workflows rely heavily on genomic identification of oncogenic driver mutations or the functional loss of tumor suppressors. These pipelines can identify single-agent treatments for patients, but monotherapy is often insufficient and can drive resistance. Recently, functional drug screening has been employed to evaluate tumor-specific drug sensitivities that complement molecular testing. We describe a resistance evaluation after first line exposure (REFLEX) multi-omic paradigm using drug-induced molecular changes to prioritize effective hits from combination screening. In KRAS-mutant cancer models, trametinib treatment caused dysregulation of the purine biosynthetic pathway driven by reductions in enzyme GART. This induced vulnerability nominated purine analog 6-thioguanine as a synergistic partner. Across diverse KRAS-mutant lineages, trametinib-induced GART loss predicts sensitivity to the combination. In vivo, the treatment significantly increases overall survival without systemic toxicity. Integrating drug-induced multi-omic changes with functional screening identifies therapeutic strategies, supporting the use of purine analogs with MEK inhibitors for KRAS-mutant tumors.
    Keywords:  Human metabolism; Oncology; Pharmacology; Precision medicine; Systems biology
    DOI:  https://doi.org/10.1016/j.isci.2026.114954
  10. J Hepatocell Carcinoma. 2026 ;13 580242
       Purpose: Radiotherapy constitutes a cornerstone in the management of hepatocellular carcinoma (HCC), but its efficacy is limited by radioresistance. Sphingolipids, a class of bioactive lipids, have been implicated in the metabolic reprogramming associated with treatment resistance. However, the potential of circulating sphingolipids as non-invasive biomarkers to predict radiosensitivity in HCC patients remains unexplored.
    Patients and Methods: This prospective study enrolled 61 HCC patients scheduled for radiotherapy (NCT06864221). Pre-treatment plasma samples were analyzed via LC-MS/MS to quantify 13 sphingolipid species. The primary endpoint was objective response rate (ORR) per mRECIST at 12 weeks. Predictive models were developed using multivariate logistic regression with forward selection and LASSO, evaluated by AUC with bootstrap validation, calibration, and decision curve analysis. Longitudinal analysis was performed in a sub-cohort (n=25) with paired pre- and post-radiotherapy plasma samples.
    Results: The objective response rate was 54.1%. Univariable analysis identified a distinct sphingolipid signature in responders, characterized by significantly lower S1P and higher levels of CER(d18:1/20:0) and CER(d18:1/24:1). These candidate biomarkers, along with significant clinical variables, were entered into multivariate modeling. The optimal integrated model (Model 1), selected via forward selection, comprised S1P, CER(d18:1/20:0), and the clinical factors ALP and TBIL, and excelled at predicting response (bootstrap-corrected AUC=0.930). A second model based on ceramide/S1P balance (CER(d18:1/26:1)/S1P, Total CER(d18:1)/S1P, AFP) also performed robustly (bootstrap-corrected AUC=0.828). Both models showed clinical utility per decision curve analysis. Longitudinal analysis revealed a coordinated metabolic shift in responders, with reduced S1P and elevated CER(d18:1/26:0), supporting a radiation-induced "sphingolipid rheostat" shift toward apoptosis.
    Conclusion: This exploratory study provides the first clinical evidence that the baseline plasma sphingolipid profile is a potent, non-invasive predictor of HCC radiosensitivity, validating the "sphingolipid rheostat" theory. Our findings establish a framework for sphingolipid-guided precision radiotherapy and lay the necessary groundwork for future large-scale, multi-center validation trials, which hold significant potential to refine patient stratification and advance the development of novel metabolism-targeted interventions.
    Keywords:  biomarker; liquid chromatography-tandem mass spectrometry; predictive model; radiotherapy
    DOI:  https://doi.org/10.2147/JHC.S580242
  11. Bioorg Med Chem Lett. 2026 Mar 03. pii: S0960-894X(26)00075-2. [Epub ahead of print]136 130608
      FLT3 mutations, including internal tandem duplications (ITD) and tyrosine kinase domain (TKD) variants, are key drivers of acute myeloid leukemia (AML) and represent attractive therapeutic targets. Guided by a scaffold-hopping strategy based on G-749 (denfivontinib), a series of quinazoline-based derivatives was designed and synthesized to explore structure-activity relationships (SAR). Among them, compound W4 showed the most promising profile, exhibiting potent antiproliferative activity against MV4-11 and MOLM-13 cells and strong inhibition of FLT3-ITD (IC50 = 16.0 nM) and FLT3-D835Y (IC50 = 20.4 nM), while displaying negligible activity toward c-KIT kinase (IC50 > 100 μM). Mechanism studies indicated that W4 induced G0/G1 cell cycle arrest and apoptosis, accompanied by a reduction in intracellular reactive oxygen species levels and a loss of mitochondrial membrane potential. Collectively, these results identified W4 as a potent FLT3 inhibitor and provided valuable SAR insights for further scaffold optimization.
    Keywords:  Antitumor activity; FLT3 inhibitor; Quinazoline derivatives; Structure optimization
    DOI:  https://doi.org/10.1016/j.bmcl.2026.130608