bims-glucam Biomed News
on Glutamine cancer metabolism
Issue of 2026–03–08
seventeen papers selected by
Sreeparna Banerjee, Middle East Technical University



  1. J Cell Commun Signal. 2026 Mar;20(1): e70064
      Glucose deprivation (Glu-D) is a critical feature of the tumor microenvironment. Under such conditions, tumor cells seek alternative metabolic resources to maintain rapid growth and proliferation. Glutamine serves as a key alternative resource for cancer cells, yet the metabolic mechanisms involving its transporters in non-small cell lung cancer remain poorly understood. Lentiviral vectors for overexpression and knockdown of phosphoenolpyruvate carboxykinase 2 (PCK2), solute carrier family 38 member 2 (SLC38A2), and CEBPB were constructed. Transwell, flow cytometry, Western blotting, and dual-luciferase reporter assays were used to investigate the regulatory relationship between PCK2 and SLC38A2 under Glu-D, as well as their effects on cellular glutamine metabolism, glycolysis, and malignant cell behaviors. PCK2 and SLC38A2 were highly expressed in human adenocarcinomas tissues. PCK2 upregulated SLC38A2 expression, though this effect was indirect. Under Glu-D, knockdown of PCK2 or SLC38A2 significantly reduced cellular glutamine utilization, inhibited glycolysis, and suppressed malignant cell behaviors. Treatment with an AMP-activated protein kinase (AMPK) inhibitor or knockdown of CEBPB produced similar effects. PCK2 activated AMPK, which increased downstream SLC38A2 expression by activating the transcription factor CEBPB. PCK2 upregulates SLC38A2 expression via the AMPK-CEBPB axis, enhancing glutamine utilization to promote glycolysis and malignant behaviors in A549 cells under Glu-D.
    Keywords:  AMPK‐CEBPB axis; NSCLC; PCK2; SLC38A2; glucose deprivation; glutamine utilization; metabolize
    DOI:  https://doi.org/10.1002/ccs3.70064
  2. J Biol Chem. 2026 Mar 04. pii: S0021-9258(26)00212-7. [Epub ahead of print] 111342
      Cancer metabolic reprogramming is a driver of tumorigenesis and progression. While extensive research has highlighted the roles of metabolic enzymes and signaling pathways in this process, the mechanisms by which chromatin regulation coordinates the metabolic network at the transcriptional level remain unclear. The SWI/SNF chromatin remodeling complex, a key epigenetic regulator, has recently been shown to modulate multiple tumor metabolic pathways. Metabolic reprogramming induced by mutations in its subunits has garnered increasing attention, but comprehensive reviews on how SWI/SNF-mediated chromatin remodeling governs this process are limited. This paper examines how the SWI/SNF complex regulates metabolic gene transcription by positioning promoters and enhancer regions, guided by transcription factors (TFs), and remodeling nucleosome structures. It further discusses its role in regulating glycolysis, the tricarboxylic acid cycle (TCA), oxidative phosphorylation (OXPHOS), lipid metabolism, and the coupling of carbon-nitrogen metabolism between amino acids and glucose-lipid metabolism. Focusing on subunit mutations such as ARID1A, SMARCA4, and PBRM1, this paper explores their impact on metabolic adaptation, offering insights for identifying therapeutic targets. Based on these findings, a combination intervention strategy targeting the protein levels of glutaminase 1 (GLS1), OXPHOS (complex I), glutamine transport, and glycolysis is proposed. By integrating SWI/SNF complex status and metabolic phenotypes, a therapeutic framework is developed that balances metabolic compensation blockade and enhanced cell death sensitivity, providing a more precise treatment strategy for metabolism-dependent tumors.
    Keywords:  Cancer metabolic reprogramming; Epigenetic regulation; Glutamine metabolism; Glycolysis; Oxidative phosphorylation; SWI/SNF complex
    DOI:  https://doi.org/10.1016/j.jbc.2026.111342
  3. J Cell Mol Med. 2026 Mar;30(5): e71070
      Most cancer cells rely on aerobic glycolysis to support uncontrolled proliferation and evade apoptosis and switch to glutamine metabolism to survive under hypoxic conditions. In hepatocellular carcinoma (HCC), the Wnt/β-catenin pathway acts as a critical driver of metabolic reprogramming and stemness, primarily by enhancing aerobic glycolysis and altering the tumour microenvironment. The Wnt/β-catenin pathway induces activation of enzymes required for glucose metabolism and regulates the expression of glutamate transporter and glutamine synthetase. The objective of this study is to examine the mechanism by which riluzole inhibits HCC growth and induces autophagy. The results indicate that riluzole inhibits cell viability and colony formation of HCC cells and cancer stem cells (CSCs) and induces apoptosis, while sparing human normal hepatocytes. Riluzole induces autophagic cell death by inducing Beclin1 and Atg5. Riluzole inhibits β-catenin, Wnt3a, Wnt5a, Axin1, TCF, LEF and GSK3β expression, and TCF/LEF activity in HCC cells. Inhibition of the Wnt-β-catenin/TCF-LEF pathway by riluzole suppresses the expression of Cyclin D1, Axin2, cMyc, MCT1 and DNMT1. Riluzole inhibits the expression of Glut1 and Glut3, PDK1, LDHA and PKM2, glucose uptake and NAD+ levels. Furthermore, riluzole inhibits glutamate release, which reduces the antioxidant glutathione, leading to increased reactive oxygen species (ROS). Riluzole disrupts mitochondrial homeostasis by increasing Bax/Bcl-2 ratio, resulting in a drop of mitochondrial membrane potential. In conclusion, riluzole inhibits HCC growth by regulating glucose and glutamine metabolism and inducing autophagic cell death, thereby highlighting its therapeutic potential for HCC treatment.
    Keywords:  Wnt; autophagy; cancer stem cells; glucose; glutamate; glutamine; hepatocellular carcinoma; metabolism; riluzole; β‐Catenin
    DOI:  https://doi.org/10.1111/jcmm.71070
  4. Adv Sci (Weinh). 2026 Mar 07. e20798
      Glutamine is an essential amino acid for tumor survival, but therapies targeting glutamine metabolism have largely failed due to adaptive resistance mechanisms. Here, we identify the pseudokinase TRIB3 as a key mediator of the metabolic adaptation of hepatocellular carcinoma (HCC) cells to limiting glutamine availability. TRIB3 is upregulated under glutamine deprivation in a c-Jun-dependent manner, functioning in the nucleus to safeguard DNA repair fidelity, allowing the timely resolution of DNA damage and preventing replication catastrophe. TRIB3 binds to G-quadruplex DNA (G4-DNA) structures throughout the genome, recruiting the helicase DDX5 to resolve them as a cooperative functional complex. Depleting TRIB3 or DDX5 in HCC cells leads to exaggerated G4-DNA accumulation and heightened DNA damage associated with the downregulation of DNA damage repair (DDR) pathways. We illustrate this effect on homologous recombination (HR) pathway genes, finding that TRIB3-DDX5 prevents G4-DNA accumulation at the BRCA1 and RAD51AP1 promoter regions that would otherwise suppress transcription. In vivo, TRIB3 silencing suppresses HCC xenograft growth, patently increasing DNA damage and apoptosis when mice were maintained on glutamine-deficient diets. Clinically, TRIB3 is overexpressed in HCC and correlates with poor prognosis. Our results propose the TRIB3-DDX5-G4 axis as a therapeutic target in HCC and other TRIB3-high malignancies.
    Keywords:  DDX5; DNA repair; G4 DNA; TRIB3; nutrient stress
    DOI:  https://doi.org/10.1002/advs.202520798
  5. J Clin Invest. 2026 Mar 02. pii: e172380. [Epub ahead of print]136(5):
      The link between glutaminolysis and osteoarthritis (OA) has only recently begun to be elucidated. Here, we report the association of obesity- and injury-induced cartilage damage with impaired glutaminolysis in chondrocytes. Defective glutaminolysis triggered the onset and progression of OA, with enhanced catabolism and decreased anabolism. Supplementation of α-ketoglutarate (αKG), a key component in glutaminolysis and an epigenetic factor, effectively protected cartilage against degradation in vivo via a TCA cycle- and HIF-1α-independent manner. Mechanistically, OA pathogenic factors increased H3K27me3 deposition on promoters of key glutaminolysis genes, including Slc1a5 and Gls1, leading to impaired glutaminolysis. Conversely, αKG facilitated Kdm6b-dependent H3K27me3 demethylation of not only glutaminolysis genes to rescue Gln metabolism but also Ube2o to reverse OA. Elevated Ube2o expression led to TRAF6 ubiquitination and subsequent inhibition of NF-κB signaling, thereby reversing the pathological reprogramming of glycolysis and oxidative phosphorylation and protecting against cartilage destruction. Collectively, these results demonstrated that OA pathogenic factors impair glutaminolysis through epigenetic regulation, which further exacerbate OA. Moreover, αKG restores metabolic homeostasis and alleviates OA through H3K27me3 demethylation.
    Keywords:  Cartilage; Inflammation; Metabolism
    DOI:  https://doi.org/10.1172/JCI172380
  6. Cell Metab. 2026 Mar 03. pii: S1550-4131(26)00046-X. [Epub ahead of print]38(3): 447-448
      In a recent issue of Cell, Gu et al. find that regulatory T (Treg) cells metabolize tumor-derived ammonia via the urea cycle and spermine synthesis, promoting immunosuppression through PPARγ-dependent oxidative phosphorylation. Inhibition of tumor glutamine metabolism reduces ammonia levels and overcomes Treg cell-mediated resistance to anti-PD-1 therapy.
    DOI:  https://doi.org/10.1016/j.cmet.2026.02.003
  7. Emerg Microbes Infect. 2026 Dec;15(1): 2622213
      Chikungunya virus (CHIKV), an emerging mosquito-borne alphavirus, induces debilitating polyarthralgia and myositis with no licensed specific therapeutic drugs. This study investigates the virological, immunological, and pathological consequences of targeting glycolysis and glutaminolysis during CHIKV infection. In vitro, either glucose/glutamine deprivation, or pharmacological inhibition by 2DG/DON significantly suppressed viral replication in mammalian cell lines. In vivo, however, differential tissue biodistribution dictated that neither inhibitor reduced viral loads in serum or foot tissues of acute infected mice following footpad inoculation with 10⁴ PFU CHIKV. Strikingly, DON, but not 2DG, abolished histopathological manifestations of myositis and inflammatory infiltration despite comparable viral burdens. Mechanistically, DON-mediated tissue protection was related to dual immunomodulation. DON significantly depleted splenic innate immune cells, including monocytes and macrophages, which play roles in driving tissue inflammatory infiltration cascades. Meanwhile, DON inhibited CD4 + and CD8+ T cell effector programmes, resulting in suppressed activation marker (CD44) expression and effector cell differentiation (decreased effector: naive ratio and TEM: TCM balance). The proliferative capacity (Ki-67 + cells), polyfunctional cytokine responses (IFN-γ+, TNF-α and IL-17 + cells) and cytotoxicity potential (CD107a + cells) of CD4 + and CD8+ T cells were significantly impaired by DON injection. Crucially, glutaminolysis inhibition uncoupled immunopathology from viral containment, attenuating tissue damaging immunity while preserving baseline antiviral competence. Collectively, these findings establish host glutamine metabolism as a pharmacologically tractable target for alphavirus-induced arthritis, demonstrating that selective immunometabolic modulation resolves the severe acute inflammatory pathology.
    Keywords:  6-diazo-5-oxo-L-norleucine; Chikungunya virus; T cell responses; glutaminolysis; immunopathology; metabolic modulation
    DOI:  https://doi.org/10.1080/22221751.2026.2622213
  8. Oral Oncol. 2026 Feb 28. pii: S1368-8375(26)00071-0. [Epub ahead of print]175 107918
       BACKGROUND: Oral squamous cell carcinoma (OSCC) exhibits significant cellular heterogeneity and metabolic reprogramming that influence tumor progression and therapeutic responses. However, the molecular mechanisms underlying these processes remain poorly understood.
    METHODS: We performed an integrated analysis of single-cell RNA sequencing and spatial transcriptomics analysis on OSCC samples to characterize cellular heterogeneity and identify key regulatory factors. Summary-data-based Mendelian randomization (SMR) analysis was conducted to establish causal links between gene expression and OSCC risk. Functional enrichment, protein-protein interaction (PPI) network analysis, molecular docking, and co-immunoprecipitation (Co-IP) were employed to elucidate molecular mechanisms.
    RESULTS: Single-cell analysis of 50,667 cells identified nine distinct cell populations with epithelial cells showing the highest glutamine metabolism activity. SMR analysis revealed glutathione S-transferase omega 2 (GSTO2) as a genetically validated protective factor for OSCC risk. GSTO2-positive epithelial cells exhibited enhanced metabolic reprogramming, particularly in fatty acid degradation and amino acid catabolism pathways. Spatial transcriptomics demonstrated that GSTO2-positive cells were spatially organized and showed enhanced communication with immune cells. Protein-protein interaction analysis identified interferon-stimulated genes (MX1, OAS1, UBE2L6) and immunoproteasome subunits (PSMB8, PSMB9) as core regulatory hubs. Molecular docking confirmed direct binding interactions between GSTO2 and these hub proteins, with MX1-GSTO2 showing the strongest binding affinity (-10.7 kcal/mol). Co-immunoprecipitation experiments validated the physical interaction between GSTO2 and MX1.
    CONCLUSIONS: This study indicates that GSTO2 defines an epithelial subset characterized by enhanced metabolic activity and immune interactions, highlighting its potential as a biomarker and therapeutic target in OSCC.
    Keywords:  GSTO2; Metabolic reprogramming; Oral squamous cell carcinoma; Single-cell RNA sequencing; Spatial transcriptomics
    DOI:  https://doi.org/10.1016/j.oraloncology.2026.107918
  9. Crit Rev Oncol Hematol. 2026 Feb 28. pii: S1040-8428(26)00119-8. [Epub ahead of print]221 105232
      Glutamine synthetase (GS), a key enzyme in nitrogen metabolism, acts as a central node by catalyzing the synthesis of glutamine from glutamate and ammonia, playing a pivotal role in maintaining cellular metabolic homeostasis. Studies have shown that GS is upregulated in various types of tumors, and its expression level is closely associated with tumor initiation, progression, and poor prognosis. This review systematically explores the multifaceted molecular mechanisms through which GS promotes malignant tumor progression. Within the tumor microenvironment, GS enhances the immunosuppressive functions of regulatory T cells (Tregs) and M2-type tumor-associated macrophages (TAMs), thereby inducing immune escape. It also promotes abnormal tumor vasculature by reprogramming metabolism and regulating key cellular behaviors involved in angiogenesis. Furthermore, GS mediates resistance to L-asparaginase and radiotherapy. It also enhances tumor invasion and metastasis via mechanisms including epithelial-mesenchymal transition (EMT). Additionally, this article summarizes potential GS-targeted therapeutic strategies, including small-molecule inhibitors and nano-drug delivery systems, offering theoretical foundations and new directions for reversing tumor drug resistance and developing novel anti-tumor therapies. By comprehensively elucidating the role of GS in multiple malignant processes-including cell proliferation, angiogenesis, invasion and metastasis, immune evasion and therapy resistance-this review aims to provide new insights into precision therapies targeting tumor metabolic reprogramming.
    Keywords:  Angiogenesis; Cell proliferation; Glutamine synthetase; Immune evasion; Invasion and metastasis; Metabolic reprogramming; Therapy resistance
    DOI:  https://doi.org/10.1016/j.critrevonc.2026.105232
  10. Mol Ther. 2026 Mar 05. pii: S1525-0016(26)00191-7. [Epub ahead of print]
      Tumor cells adapt to therapeutic stress by preserving mitochondrial integrity through mitophagy, but excessive mitophagy can overwhelm this adaptative mechanism and precipitate mitochondrial collapse. Here, we demonstrate that 1,25-dihydroxyvitamin D3 (1,25D3) reduces glioblastoma resistance to the standard chemotherapeutics temozolomide by driving mitophagic overload and mitochondrial dysfunction. We identified mitochondrial sirtuin SIRT4 as a key downstream effector of mitochondrial metabolism and quality control triggered by 1,25D3-induced mitochondrial stress. Pharmacological levels of 1,25D3 activate mitophagy by transcriptionally upregulating SIRT4 through vitamin D receptor (VDR) signaling. SIRT4, which is frequently downregulated in glioblastoma, suppresses glioblastoma glutamine metabolism by inhibiting glutamate dehydrogenase activity and limiting α-ketoglutarate availability, thereby integrating metabolic stress with enhanced mitophagy. This VDR-SIRT4 axis shifts mitophagy from a cytoprotective process to a lethal pathway, selectively sensitizing tumor cells while sparing normal astrocytes and brain tissue. By exploiting mitochondrial quality control as a metabolic vulnerability, 1,25D3 enhances chemotherapeutic efficacy and provides a translational rationale for repurposing 1,25D3 in resistant glioblastoma.
    DOI:  https://doi.org/10.1016/j.ymthe.2026.03.006
  11. IUBMB Life. 2026 Mar;78(3): e70091
      Endoplasmic reticulum glycosyltransferase ALG8 controls metabolic fate in autosomal dominant polycystic kidney disease (ADPKD). In this paper, we summarize human genetics, cell-based, and organ-based evidence to investigate whether ALG8 variants affect cyst initiation and metabolic states of ADPKD. Population screening showed ALG8 variant enrichment in ADPKD cohorts (OR = 9.75, P0.001); loss-of-function alleles interact with PKD1 mutations to accelerate cystogenesis. ALG8 deficiency leads to metabolic collapse by several mechanisms. Impaired polycystin-1 glycosylation disrupts ER-to-cilium trafficking, prevents PC1/PC2 complex assembly, and impedes calcium-dependent ATP production. Deficient LRP6 glycosylation activates Wnt/-catenin signaling. This shifts metabolism toward aerobic glycolysis, leading to Warburg-like reprogramming seen in malignancy. Single cell analysis showed ALG8 deficient cystic epithelium has tumor-like metabolic signatures, such as increased glucose uptake, suppressed oxidative phosphorylation, and glutamine dependence. Chemical chaperones that restore folding capacity or glycosylation inhibitors that lower anabolic demand both suppressed cyst formation in ALG8/PKD1-deficient organoids. The connection from ALG8 loss to "oncogenic-like" metabolism remains incomplete. Study-to-study variability in model system, genotype, and endpoint still limits cross-cohort comparison. This dual vulnerability-of protein folding and glycosylation-is due to the fragile metabolic balance in cystogenesis. These results recast ADPKD as a metabolic disorder where glycosylation defects link ciliary dysfunction to oncogenic transformation. We focus on three areas: (i) convergence with multiple lines of evidence, (ii) disagreement, and (iii) testable predictions for future studies and trials. The overlap between cystogenic and tumorigenic metabolic programs suggests cancer metabolic inhibitors may be reused for ADPKD in near-term translation. By defining ALG8 as a metabolic checkpoint in polycystic disease, we uncover targets at the glycosylation-metabolism interface.
    Keywords:  ALG8 glycosyltransferase; N‐glycosylation; Warburg effect; autosomal dominant polycystic kidney disease (ADPKD); metabolic reprogramming
    DOI:  https://doi.org/10.1002/iub.70091
  12. Nat Cell Biol. 2026 Mar 06.
      How cancer cells couple metabolic stress sensing to orchestrate specific survival programmes is a key question. Here we show a long non-coding RNA (lncRNA)-guided epitranscriptomic mechanism orchestrating metabolic adaptation by controlling the stability of master stress regulator ATF4. Glucose or glutamine deprivation induces endoplasmic reticulum stress via reactive oxygen species-NRF2-dependent transcription of the lncRNA DAMER. Following its demethylation and nuclear retention by the m6A-eraser ALKBH5, DAMER acts as a scaffold, guiding ALKBH5 to demethylate and stabilize ATF4 mRNA through specific base-pairing. This provides an alternative post-transcriptional pathway for ATF4 upregulation, rewiring asparagine metabolism to promote cancer cell survival under stress. Furthermore, we identified the US FDA-approved drug elbasvir as a potent inhibitor of the DAMER-ALKBH5 interaction. Elbasvir dismantles this adaptive programme, targeting tumour asparagine dependency and exhibiting potent antitumour effects in preclinical models. Our findings reveal a paradigm for lncRNA-guided RNA demethylation that solves a target specificity enigma and offers a strategy targeting metabolic adaptation in cancer.
    DOI:  https://doi.org/10.1038/s41556-026-01905-z
  13. Acta Neuropsychiatr. 2026 Mar 05. 1-17
       OBJECTIVE: Investigating metabolic differences between pre-pubertal Flinders sensitive (FSL) and resistant (FRL) line rats and determine the impact of early-life adversity on these differences.
    METHODS: Untargeted metabolomic profiling of whole-brain tissue from postnatal day 25 Flinders line rats, exposed to maternal separation with early weaning (MSEW), or not, was done by using gas chromatography time-of-flight mass spectrometry (GC-TOF-MS).
    RESULTS: Irrespective of MSEW, FSL rats had higher urea and lower glutamine, norvaline and valine concentrations than age-matched FRL controls. Across strains, MSEW reduced gamma-aminobutyric acid (GABA), glutamate, glutamine, lactate, phenylalanine, norvaline and valine concentrations, whist elevating 2-keto-3-methylbutyric acid, glycerophosphate, and urea. This effect was most pronounced in FRL rats.
    CONCLUSION: Pre-pubertal FSL rats displayed distinct metabolic signatures associated with altered energy and amino acid metabolism. Early-life stress further disrupts these pathways, highlighting key metabolites as potential targets in the expansion of the biological contracts underlying the pre-pubertal FSL/FRL model.
    Keywords:  Adverse childhood experiences; Depressive Disorder; Metabolomics; Rats; Stress
    DOI:  https://doi.org/10.1017/neu.2026.10066
  14. 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
  15. Cancer Lett. 2026 Mar 02. pii: S0304-3835(26)00159-X. [Epub ahead of print]645 218396
      Angiogenesis fuels colorectal cancer (CRC) growth and metastasis by supplying oxygen and nutrients to expanding tumors. Here, we define a TGM2-mediated serotonylation axis in tumor endothelial cells as a driver of angiogenesis and a key mediator of epigenetic reprogramming within the tumor microenvironment. Across CRC single-cell datasets, TGM2 is broadly expressed in endothelial cells, and endothelial TGM2 correlates with the H3Q5Ser mark. Endothelial-specific deletion of Tgm2 in mice markedly suppresses angiogenesis and slows allograft tumor growth. In human umbilical vein endothelial cells, TGM2 knockdown diminishes H3Q5Ser, proliferation, migration, and tube formation, which can be rescued with nuclear-localized wild-type TGM2 but not a transamidase-inactive mutant. Mechanistically, TGM2-catalyzed serotonylation promotes LDHA transcription via H3Q5Ser at the LDHA promoter, thereby upregulating glycolysis. Hypoxia induces TGM2 expression via HIF-1α signaling. Moreover, endothelial cells lack canonical serotonin transporters and serotonin biosynthesis, and exosome-mediated transfer of 5-HT provides a source that fuels endothelial serotonylation. Clinically, high endothelial TGM2 and H3Q5Ser levels predict poorer prognosis. Collectively, the TGM2-serotonylation axis in endothelial cells represents a promising therapeutic target to disrupt tumor angiogenesis and CRC progression, with potential to synergize with immunotherapy by normalizing tumor vasculature and enhancing anti-tumor immunity.
    Keywords:  Serotonylation; Transglutaminases; Tumor angiogenesis; Tumor-associated endothelial cells
    DOI:  https://doi.org/10.1016/j.canlet.2026.218396
  16. Metabolomics. 2026 Mar 06. pii: 32. [Epub ahead of print]22(2):
       INTRODUCTION: Gliomas represent the tumors of the central nervous system that originate from glial cells. Overall survival predictions and treatment regimen selection are based on accurate tumor diagnosis and grading. However, the diagnosis of glioma remains critically dependent on either invasive biopsies or advanced imaging.
    OBJECTIVE: This exploratory study aims to assess the diagnostic potential of urine specimens for discriminating gliomas from controls and identify the dysregulated pathways in a North Indian cohort. Urine is an ideal non-invasive candidate, requires no prior preparation, and considerably increases patient compliance.
    METHOD: Urine samples from 50 glioma patients were analysed with 1H NMR (Nuclear Magnetic Resonance) spectroscopy and compared with those of healthy controls. Statistical analysis was performed in MetaboAnalyst 6.0 to identify significantly perturbed metabolites. Diagnostic performance was assessed using the Receiver Operating Characteristic (ROC) curve, and the Random Forest model was used to evaluate classification accuracy. Pathway enrichment and topology analysis based on the KEGG (Kyoto Encyclopedia of Genes and Genomes) database were performed to identify dysregulated pathways.
    RESULTS: 1H NMR metabolic analysis of urine samples revealed seven statistically significant (p < 0.05) metabolites namely acetate, pyruvate, creatinine, dimethylamine, glutamine, alanine and carnitine. This panel of metabolites displayed excellent diagnostic capability with an Area Under the Curve of 0.90 as measured by a multivariate ROC curve. The random forest model efficiently differentiated glioma from control samples using significant metabolites. Disruption in the primary energy pathways of the body and in the metabolism of major amino acids was observed in the pathway analysis.
    CONCLUSION: Integration of these urinary signatures into current clinical practice can serve as an additional diagnostic tool and a non-invasive screening method for populations at risk. They can also be monitored in real time, thus aiding in adaptive treatment strategies and therapy assessment.
    Keywords:  Cancer; Glioma; Metaboanalyst; Metabolomics; Nuclear magnetic resonance (NMR)
    DOI:  https://doi.org/10.1007/s11306-026-02414-8
  17. NPJ Sci Food. 2026 Mar 02.
      Although cellular senescence in pulmonary epithelial cells is a recognized driver of chronic lung diseases, the role of dietary factors in initiating this process remains poorly defined. Here, we identify monosodium glutamate (MSG), the primary source of umami taste, as a trigger of a novel dietary-lung axis. We demonstrate that chronic intake of high amounts of MSG elevates pulmonary L-glutamic acid (Glu) levels, which activate an NMDAR-miMOMP signaling cascade in pulmonary epithelial cells, leading to cellular senescence and lung injury. This mechanism is consistent across multiple high-Glu diets, including high-fat and high-protein regimens. Furthermore, we demonstrate that high-Glu diets exacerbate pulmonary fibrosis progression by increasing the senescence burden. Our findings suggest that dietary Glu is a modifiable risk factor for chronic lung diseases and reveal that the NMDAR-miMOMP-senescence axis is a potential therapeutic target for metabolic respiratory syndromes.
    DOI:  https://doi.org/10.1038/s41538-026-00783-x