bims-medica Biomed News
on Metabolism and diet in cancer
Issue of 2025–09–21
24 papers selected by
Brett Chrest, Wake Forest University



  1. Cancer Med. 2025 Sep;14(18): e71244
       BACKGROUND: Cancer metabolism is a field focused on the unique alterations in metabolic pathways that occur in cancer cells, distinguishing them from the metabolic processes in normal cells.
    METHODS: An extensive review of the current literature on the metabolic adaptation of cancer cells was carried out in the current study.
    RESULTS: The rapidly proliferating cells require high levels of molecules, such as glucose, amino acids, lipids, and nucleotides, along with increased energy demand (ATP). These requirements are met through alterations in the processes involving glucose, amino acid, lipid, and nucleotide metabolism. Modifications in glucose metabolism in cancer cells involve changes in glucose uptake, glycolysis, the pentose phosphate pathway, and the tricarboxylic acid cycle. Similarly, alterations in amino acid metabolism in cancer cells relate to upregulated amino acid transport and glutaminolysis. Cancer cells also have increased lipid intake from the extracellular microenvironment, upregulated lipogenesis, and enhanced lipid storage and mobilization from intracellular lipid droplets. These rapidly proliferating cells also achieve their increased demand for nucleotides by changing the expression of enzymes in the salvage and de novo nucleotide pathways. Consequently, these metabolic processes are targets for developing cancer therapeutics. However, it is important to note that the metabolic changes in cancer cells can also contribute to resistance against various cancer therapies.
    CONCLUSION: This review will explore the various ways in which cancer cells reprogram metabolic processes to sustain rapid proliferation and survival. The information presented in this report could help in the therapeutics designed to target them, and the challenges of cancer drug resistance arising from these metabolic adaptations.
    Keywords:  Warburg effect; cancer metabolism; drug resistance; glucose metabolism; nucleotide metabolism; therapeutics
    DOI:  https://doi.org/10.1002/cam4.71244
  2. Cell Metab. 2025 Sep 16. pii: S1550-4131(25)00381-X. [Epub ahead of print]
      Acute myeloid leukemia (AML) commonly relapses after initial chemotherapy response. We assessed metabolic adaptations in chemoresistant cells in vivo before overt relapse, identifying altered branched-chain amino acid (BCAA) levels in patient-derived xenografts (PDXs) and immunophenotypically identified leukemia stem cells from AML patients. Notably, this was associated with increased BCAA transporter expression with low BCAA catabolism. Restricting BCAAs further reduced chemoresistant AML cells, but relapse still occurred. Among the persisting cells, we found an unexpected increase in protein production. This was accompanied by elevated translation of 2-oxoglutarate- and iron-dependent oxygenase 1 (OGFOD1), a known ribosomal dioxygenase that adjusts the fidelity of tRNA anticodon pairing with coding mRNA. We found that OGFOD1 upregulates protein synthesis in AML, driving disease aggressiveness. Inhibiting OGFOD1 impaired translation processing, decreased protein synthesis and improved animal survival even with chemoresistant AML while sparing normal hematopoiesis. Leukemic cells can therefore persist despite the stress of chemotherapy and nutrient deprivation through adaptive control of translation. Targeting OGFOD1 may offer a distinctive, translation-modifying means of reducing the chemopersisting cells that drive relapse.
    Keywords:  BCAA; OGFOD1; Ribo-seq; acute myeloid leukemia; chemoresistance; metabolism; protein biosynthesis; ribosome pausing; translation accuracy
    DOI:  https://doi.org/10.1016/j.cmet.2025.08.008
  3. bioRxiv. 2025 Sep 04. pii: 2025.08.30.673205. [Epub ahead of print]
      Mutations in isocitrate dehydrogenase (IDHm) define a distinct molecular class of gliomas. IDHm converts α-ketoglutarate (α-KG) to the oncometabolite D-2-hydroxyglutarate (D-2HG), which drives tumorigenesis. The IDHm inhibitor vorasidenib suppresses D-2HG production and extends progression-free survival in some, but not all, IDHm glioma patients. Here, using clinically relevant patient-derived IDHm models and patient tissue, we show that phosphoglycerate dehydrogenase (PHGDH) drives intrinsic resistance to vorasidenib by promiscuously converting α-KG to D-2HG and maintaining D-2HG concentration despite IDHm inhibition. Silencing PHGDH sensitizes resistant models to vorasidenib, while conversely, overexpressing PHGDH induces vorasidenib resistance in sensitive models. Importantly, deuterium metabolic imaging of D-2HG production from diethyl-[3,3'- 2 H]-α-ketoglutarate provides an early readout of response and resistance to vorasidenib that is not available by anatomical imaging in vivo. Collectively, we have identified PHGDH-driven D-2HG production as an intrinsic mechanism of resistance to vorasidenib and diethyl-[3,3'- 2 H]α-ketoglutarate as a non-invasive tracer for interrogating intrinsic resistance in IDHm gliomas.
    STATEMENT OF SIGNIFICANCE: Vorasidenib, which suppresses D-2HG production, is the first precision therapy to be approved for IDHm glioma patients. We show that PHGDH-driven restoration of D-2HG production mediates intrinsic resistance to vorasidenib in IDHm gliomas. Importantly, deuterium metabolic imaging of D-2HG production from diethyl-[3,3'- 2 H]-α-ketoglutarate enables non-invasive assessment of resistance in IDHm gliomas.
    DOI:  https://doi.org/10.1101/2025.08.30.673205
  4. EMBO Rep. 2025 Sep 16.
      During prolonged starvation and exhaustive exercise, when there is low availability of carbohydrates, the liver breaks down fatty acids to generate ketone bodies, which are utilized by peripheral tissues as an alternative fuel source. The transcription factor MEF2D undergoes regulated alternative splicing in the postnatal period to produce a highly conserved, muscle specific MEF2Dα2 protein isoform. Here, we discover that compared to WT mice, MEF2Dα2 exon knockout (Eko) mice display reduced running capacity and muscle expression of all three ketolytic enzymes: BDH1, OXCT1, and ACAT1. MEF2Dα2 Eko mice consistently show increased blood ketone body levels in a tolerance test, after exercise, and when fed a ketogenic diet. Lastly, using mitochondria isolated from skeletal muscle, Eko mice show reduced ketone body utilization compared to WT mice. Collectively, our findings identify a new role for the MEF2Dα2 protein isoform in regulating skeletal muscle ketone body oxidation, exercise capacity, and systemic ketone body levels.
    Keywords:  Alternative Splicing; Ketone Body; MEF2 Transcription Factors; MExercise Metabolism
    DOI:  https://doi.org/10.1038/s44319-025-00578-3
  5. Support Care Cancer. 2025 Sep 19. 33(10): 863
       PURPOSE: Intermittent fasting holds potential for improving cancer patient outcomes by promoting cancer cell death. Additionally, it depletes hepatic glycogen reserves, facilitating the release of fatty acids and ketones, which may enhance cancer cells sensitivity to chemotherapy and impede their proliferation. However, clinical data on fasting among cancer patients remain scarce. This systematic review intends to provide an overview of the impact of intermittent fasting on the safety, feasibility, tolerability, and metabolic effects of chemotherapy and targeted therapies in cancer patients.
    METHODS: Articles were retrieved from 1990 to March 2025, employing a defined search equation. Established endpoints included cancer development, treatment efficacy, side effects related to chemotherapy and targeted therapies, quality of life, and fasting tolerance. Risk of bias was assessed, utilizing a validated assessment tool.
    RESULTS: Among 1,725 articles, nine met our inclusion criteria. Risk of bias was low to moderate. These studies included patients predominantly with breast cancer (n = 258/354). Even though the safety and feasibility of intermittent fasting were confirmed, no impact on treatment outcomes and chemotherapy-related toxicities was demonstrated. However, a consistent trend emerged in reduced insulin and IGF-1 levels, along with increased erythrocyte levels among fasting patients. Three studies reported no significant difference in body weight and BMI.
    CONCLUSION: Current evidence indicates that intermittent fasting is both safe and feasible. However, due to the lack of robust evidence, a definitive conclusion regarding the impact of intermittent fasting on treatment effectiveness and side effects related to chemotherapy and targeted therapies in cancer patients cannot be drawn. Larger randomized controlled trials are warranted to validate intermittent fasting as an adjunctive therapeutic approach.
    Keywords:  Antineoplastic combined chemotherapy protocols; Caloric restriction; Carcinoma; Dietary restriction; Malignancy; Neoplasm; Targeted anticancer agents
    DOI:  https://doi.org/10.1007/s00520-025-09907-7
  6. ACS Med Chem Lett. 2025 Sep 11. 16(9): 1814-1824
      A novel nucleoside analogue, LCB-2151, has been developed to induce cell death in KRAS-mutated pancreatic human cancer cell lines, which exhibit partial resistance to gemcitabine, a widely used anticancer drug. LCB-2151 disrupts the two primary sources of ATP production, namely, glycolysis and mitochondrial oxidative phosphorylation, reducing the bioenergetic capacity of these cells and inducing the formation of reactive oxygen species. Metabolomics and mitochondrial respiration analyses reveal that LCB-2151 inhibits key enzymes in glycolysis, the TCA cycle, and fatty acid β-oxidation. These findings highlight a coordinated mechanism driving bioenergetic disruption and cell death.
    Keywords:  KRAS; Pancreatic ductal adenocarcinoma; nucleoside analogues; stereogenic all-carbon quaternary center
    DOI:  https://doi.org/10.1021/acsmedchemlett.5c00378
  7. Mol Oncol. 2025 Sep 16.
      Relapsed/refractory (R/R) disease is a major hurdle to long-term survival of acute myeloid leukemia (AML) patients treated with intensive cytarabine (AraC)-based chemotherapy. R/R AML salvage treatment with venetoclax (VEN) + azacitidine (AZA) results in overall response rates between 20% and 60%, and responses are not durable, highlighting the need for new therapies. Here, we report elevated mTORC1 signaling in AraC-resistant AML cell lines, primary AML patient samples, and patient-derived xenograft (PDX) AML cells derived from patients at relapse postchemotherapy. The CDK9 inhibitor AZD4573 suppresses mTORC1 signaling and downregulates c-MYC and MCL-1, inducing AraC-resistant AML cell death. AZD4573 in combination with VEN + AZA significantly increases AML cell death compared to any of the two-drug combinations and suppresses AML progenitor cells but spares normal hematopoietic progenitor cells. The efficacy of this triple combination remains even with a 10-fold reduction of VEN concentration. The roles of MCL-1 and c-MYC in the three-drug combination were confirmed by knockdown. This study demonstrates that AZD4573 enhances the activity of VEN + AZA against AraC-resistant AML by downregulating c-MYC and MCL-1 and to a lesser extent cellular respiration.
    Keywords:  AZD4573; acute myeloid leukemia; azacitidine; venetoclax
    DOI:  https://doi.org/10.1002/1878-0261.70124
  8. Front Hematol. 2025 ;pii: 1550681. [Epub ahead of print]4
       Background: Multiple myeloma (MM) is the second most common blood cancer after leukemia in adults. Despite advancements in treatment that have extended survival, MM remains incurable and the cancer and its treatment result in adverse acute, long-term and latent side-effects, necessitating a focus on strategies to attenuate these side-effects and improve quality of life. This narrative review highlights MM patient preferences for exercise and/or diet interventions relative to complete and ongoing interventions to identify gaps and needs for future lifestyle interventions in MM patients aimed at improving MM survivorship care.
    Methods: This updated review was completed using a comprehensive search that was conducted using PubMed and ClinicalTrials.gov databases using keywords related to MM, exercise, physical activity, diet, nutrition and patient preferences. Studies involving adults diagnosed with MM were included.
    Results: Among published studies, there are five exercise interventions and four diet and nutrition observational studies. The importance of individualized exercise interventions tailored to MM patients' needs was emphasized. Supervised exercise interventions showed higher adherence and engagement compared to unsupervised interventions. Observational diet/nutrition studies demonstrated that decreased gut microbiome diversity post-transplant is linked to poorer outcomes. Additionally, nutritional status and dietary patterns, such as high-carbohydrate and plant-based diets, can significantly impact clinical outcomes in MM patients, including sustained minimal residual disease negativity. Current clinical trials are primarily focused on feasibility and adherence, with a limited emphasis on long-term outcomes. In ClinicalTrials.gov, there are six ongoing exercise interventions, with an additional seven that are completed with no published results, one suspended trial and one active but not recruiting. Additionally, there are two combined diet and exercise interventions that are currently recruiting, with one active but no longer recruiting. Among diet and nutrition ongoing trials, there are currently two actively recruiting, two completed with no primary paper published and one study that was withdrawn.
    Discussion: These findings underscore the need for more comprehensive, long-term and adequately powered studies on the impact of exercise and diet interventions in MM patients. Patient education and empowerment within these trials are crucial for enhancing engagement and adherence to these interventions.
    Keywords:  Diet and Nutrition; Exercise; Gut Microbiome; Multiple Myeloma; Patient Preferences
    DOI:  https://doi.org/10.3389/frhem.2025.1550681
  9. Front Mol Biosci. 2025 ;12 1648209
       Background: Hemoglobin-based oxygen carriers (HBOCs) also known as blood substitutes were developed by chemical or genetic alterations of cell-free human or bovine Hbs to prolong the circulation time of Hb and to improve its ability to unload oxygen. However, toxicity and safety issues led to the termination of several clinical trials. The most persistent observation was the development of cardiac lesions after transfusion of some HBOCs in animal models. Oxidation of HBOCs in circulation, subsequent heme release and cellular uptake are thought to play an important role in the overall toxicity of HBOCs.
    Methods: We examined the effects of different redox states, ferrous (Fe+2), ferric (Fe+3) and ferryl (Fe+4) of four different HBOCs on cardiomyocyte integrity and mitochondrial respiration. The HBOC formulations used in this study were two-human derived and two bovine-derived molecules. We analyzed cellular and subcellular impacts of these forms including mitochondrial electron transport chain (ETC.) complexes individually by measuring the enzymatic activities of Complex I, Complex II-III, and Complex IV.
    Results: The ferrous, and ferric forms of these HBOCs generally induced minimum lactate dehydrogenase (LDH) release from human cardiac myocytes (AC16). Meanwhile higher oxidation state, ferryl forms of all HBOCs generated substantial cell injury as measured by LDH levels. We examined the effects of these redox forms of HBOCs and their ability to impair bioenergetic function of cultured AC16 cells. The ferrous forms of HBOCs did not cause measurable impairment of mitochondrial ETC functions, whereas ferric non-functional versions of all the HBOCs caused a significant loss of Complex IV activity but not Complex I or II-III in those cardiac cell lines. On the other hand, complex I, II-III and IV activities were completely blunted by the ferryl forms of HBOCs.
    Conclusion: This study for the first time investigated the impact of different chemical modifications on the redox activities of HBOCs towards mitochondrial complexes in cardiac myocytes. Higher oxidation ferryl states once formed trigger cellular and subcellular changes in cardiac myocytes. Our findings on the impact of HBOC redox states on mitochondrial function may therefore inform future design of alternative molecular entities to ensure safety and minimize toxicity.
    Keywords:  cardiac AC16; cytotoxicity; hemoglobin-based oxygen carriers (HBOCs); mitochondrial fractions; redox reactions
    DOI:  https://doi.org/10.3389/fmolb.2025.1648209
  10. Ther Adv Hematol. 2025 ;16 20406207251372770
       Background: Azacitidine (AZA) plus venetoclax (VEN) has emerged as a widely accepted treatment option for acute myeloid leukemia (AML), particularly in older patients or those unfit for intensive chemotherapy. However, real-world data on AZA + VEN efficacy and safety in Southeast Asia remain limited.
    Objectives: To evaluate the real-world effectiveness and safety of AZA + VEN in newly diagnosed (ND) and relapsed/refractory (R/R) AML patients in Thailand.
    Design: A retrospective observational multicenter study.
    Methods: This is a multicenter retrospective study included ND and R/R AML patients treated between 2021 and 2024 at three tertiary hospitals in Thailand. All patients received AZA at 75 mg/m2 for 7 days per cycle. VEN dosing and duration were individualized based on physician judgment, drug availability, and patient affordability. Data collection included clinical characteristics, cytogenetics, treatment details, response rates, survival outcomes, and toxicities.
    Results: A total of 81 patients were analyzed, included 54 ND and 27 R/R AML cases, with a median age of 65 years. Based on European LeukemiaNet 2022 classification, 51.9% had intermediate risk, and 33.3% had adverse risk. The composite complete remission was 56.8% (ND: 64.8%, R/R: 40.7%). VEN was administered at a median dose of 100 mg for 28 days, combined with potent CYP3A4 inhibitor of antifungal prophylaxis (posaconazole 51.0%, voriconazole 30.4%, itraconazole 17.7%). The median overall survival was 9.2 months and relapse-free survival was 8.1 months. Grades 3-4 neutropenia and febrile neutropenia occurred in 93.8% and 60.5% of patients, respectively.
    Conclusion: This real-world practice highlights the feasibility and effectiveness of AZA-VEN in combination with antifungal prophylaxis for elderly or unfit AML patients in resource-limited countries. However, infectious complications remain a concern with this low-intensity regimen.
    Keywords:  acute myeloid leukemia; azacitidine; real-world data; venetoclax
    DOI:  https://doi.org/10.1177/20406207251372770
  11. Anticancer Agents Med Chem. 2025 Sep 16.
      Isocitrate Dehydrogenases (IDH) are ubiquitous enzymes essential for cellular metabolism, including the Krebs cycle, glutamine metabolism, lipogenesis, and redox balance. Mutations in IDH1 and IDH2 are implicated in several tumors - gliomas, Acute Myeloid Leukemia (AML), cholangiocarcinoma - altering enzyme activity and causing the overproduction of 2-hydroxyglutarate (2-HG). This oncometabolite disrupts α-KGdependent proteins, impairing key processes such as differentiation, division, and DNA repair. Understanding these genetic, biochemical, and clinical aspects has made IDH enzymes promising therapeutic targets, prompting the development of targeted inhibitors for tumors harboring IDH1 or IDH2 point mutations. Selective inhibitors like ivosidenib (AG-120) and enasidenib (AG-221), targeting mutant IDH1 and IDH2 respectively, block 2- HG production and induce differentiation, achieving clinical success - particularly in AML. However, resistance due to secondary mutations, especially in the allosteric binding site, remains a major obstacle. In response, novel approaches have emerged, such as covalent inhibitors like LY3410738, which irreversibly bind mutant residues, and dual inhibitors like vorasidenib (AG-881), which act on both IDH1 and IDH2 mutations and penetrate the blood-brain barrier for treating solid tumors. Still, many clinical factors must be considered. This review explores the current landscape of IDH-targeted therapies, emphasizing the need for novel inhibitors and highlighting innovative strategies, including the design of smaller, more potent molecules with favorable pharmacokinetics and the potential of drug repositioning. We underscore that discovering new antitumor compounds targeting IDH requires a collaborative effort across biomedical fields. These advancements aim to overcome resistance, broaden therapeutic options, and improve the effectiveness of IDH-targeted treatments.
    Keywords:  IDH inhibitors; IDH mutations.; enasidenib; isocitrate dehydrogenase; ivosidenib; target therapy
    DOI:  https://doi.org/10.2174/0118715206382095250908095950
  12. FEBS Open Bio. 2025 Sep 19.
      Tryptophan (Trp) is the largest and most structurally complex amino acid, yet it is the least abundant in the proteome. Its distinct indole ring and high carbon content allow it to give rise to several biologically active metabolites, including serotonin, kynurenine (Kyn), and indole-3-pyruvate (I3P). Dysregulation of Trp metabolism has been implicated in a range of diseases, from depression to cancer. Investigating Trp and its metabolites in healthy tissues provides insight into how disease-associated disruptions may be targeted selectively while preserving essential physiological functions. Whereas previous studies have typically focused on individual organs or single metabolic branches, our analysis spans 12 peripheral organs, the central nervous system, and serum in male and female (C57BL/6) mice across three life stages: young (3 weeks), adult (54 weeks), and aged (74 weeks). We identified striking tissue-, sex-, and age-specific differences in Trp metabolism, including elevated levels of I3P and Kyn, both linked to tumor growth, in aging males. We also compared Trp metabolite profiles in tissues from mice fed a control defined diet versus a Trp-deficient diet for three weeks. This intervention led to a marked reduction in circulating Trp and its metabolites, with more modest effects observed in the liver and central nervous system. These findings underscore the importance of organ-specific and diet-sensitive analyses of Trp metabolism for understanding its role in both normal physiology and disease. Establishing baseline levels of Trp metabolites across tissues may also provide a foundation for identifying organ-specific metabolic reprogramming in cancer and other illnesses.
    Keywords:  atlas; indole‐3‐pyruvate; kynurenine; metabolism; serotonin; tryptophan
    DOI:  https://doi.org/10.1002/2211-5463.70123
  13. bioRxiv. 2025 Sep 08. pii: 2025.09.04.673818. [Epub ahead of print]
      Cytotoxic chemotherapy remains the standard-of-care treatment for patients with pancreatic ductal adenocarcinoma (PDAC). However, chemotherapy only has modest effects at improving patient survival due to primary or rapidly acquired chemoresistance. The biological underpinnings of PDAC therapy resistance are incompletely defined, but the tumor microenvironment is known to be a major contributor to chemoresistance. We have found chemoresistance is imprinted on PDAC cells by the tumor microenvironment and persists for a period of days after PDAC cells are removed from tumors. However, PDAC chemoresistance is lost upon long term culture in standard laboratory conditions. Interestingly, culture of PDAC cells in Tumor Interstitial Fluid Medium (TIFM), a culture medium we developed to recapitulate the nutrient availability of the tumor microenvironment, maintains PDAC cells in a chemo- and targeted therapy resistant state even after long term culture ex vivo . These findings suggest that microenvironmental metabolic stress keeps PDAC cells in a physiologically relevant, therapy resistant cell state that standard culture models fail to maintain. Using TIFM culture, we sought to understand how PDAC cells in this state resist therapeutic challenge. We found that chemo- and targeted therapies largely retain on-target activity within TIFM medium but fail to activate cell death, enabling a "chemotolerant" cell state, which is also observed in PDAC tumors. This chemotolerant state is driven by suppression of apoptotic priming and can be overcome by targeting the anti-apoptotic regulator BCL-XL. Taken together, these findings suggest that reprogramming of cell death mechanisms by the PDAC nutrient microenvironment is a key contributor to therapy resistance in this disease.
    DOI:  https://doi.org/10.1101/2025.09.04.673818
  14. Nat Metab. 2025 Sep 19.
      The consumption of sugar-sweetened beverages (SSBs), which contain high levels of fructose and glucose, has been causally and mechanistically linked to an increased risk of colorectal cancer (CRC). However, the effects of SSB consumption on advanced stages of disease progression, including metastasis, remain poorly understood. Here we show that exposure of CRC cells to a glucose and fructose formulation-reflecting the composition of both high-fructose corn syrup and sucrose found in SSBs-enhances cellular motility and metastatic potential compared to glucose alone. Given that CRC cells grow poorly in fructose alone, and cells in vivo are not physiologically exposed to fructose without glucose, we excluded the fructose-only condition from our studies unless needed as a control. Mechanistically, the combination of glucose and fructose elevates the NAD⁺/NADH ratio by activation of the reverse reaction of sorbitol dehydrogenase in the polyol pathway. This redox shift relieves NAD⁺ limitations and accelerates glycolytic activity, which in turn fuels activation of the mevalonate pathway, ultimately promoting CRC cell motility and metastasis. Our findings highlight the detrimental impact of SSBs on CRC progression and suggest potential dietary and therapeutic strategies to mitigate metastasis in patients with CRC.
    DOI:  https://doi.org/10.1038/s42255-025-01368-w
  15. Nat Chem Biol. 2025 Sep 15.
      The lipid composition of cells varies widely across organelles and between individual membrane leaflets. Transport proteins are thought to generate this heterogeneity, but measuring their functions in vivo has been hampered by limited tools for imaging lipids at relevant spatial resolutions. Here we present fluorogen-activating coincidence encounter sensing (FACES), a chemogenetic tool capable of quantitatively imaging subcellular lipid pools and reporting their transbilayer orientation in living cells. FACES combines bioorthogonal chemistry with genetically encoded fluorogen-activating proteins (FAPs) for reversible proximity sensing of conjugated molecules. We first apply this approach to identify roles for lipid transfer proteins that traffic phosphatidylcholine pools between the ER and mitochondria. We then show that transmembrane domain-containing FAPs can reveal the membrane asymmetry of multiple lipid classes in the trans-Golgi network and be used to investigate the mechanisms that generate it. Finally, we present that FACES can be applied to measure glycans and other molecule classes.
    DOI:  https://doi.org/10.1038/s41589-025-02021-z
  16. J Oncol Res Ther. 2025 ;pii: 10299. [Epub ahead of print]10(3):
      Glioblastoma (GBM) is the most common and aggressive primary brain cancer in adults. While chemo- and radiotherapy are often effective in treating newly diagnosed GBM, increasing evidence suggests that treatment-induced metabolic alterations promote tumor recurrence and further resistance. In addition, GBM tumors are typically hypoxic, which further contributes to treatment resistance. Recent studies have shown that changes in glioma cell metabolism driven by a shift in the isoform expression of mitochondrial cytochrome c oxidase (CcO) subunit 4 (COX4), a key regulatory subunit of mammalian CcO, may underlie the treatment-induced metabolic alterations in GBM cells. However, the impact of hypoxia on GBM energetics is not fully understood. Using isogenic GBM cell lines expressing either COX4-1 or the alternative COX4 isoform, COX4-2, we found that COX4-1 expressing cells maintained a more oxidative metabolism under hypoxia, characterized by increased CcO activity and ATP production, enhanced assembly of CcO-containing mitochondrial supercomplexes, and reduced superoxide production. Furthermore, COX4-1 expression was sufficient to increase radioresistance under hypoxic conditions. Untargeted metabolomic analysis revealed that the most significantly upregulated pathways in COX4-1-expressing cells under hypoxia were purine and methionine metabolism. In contrast, COX4-2-expressing cells showed increased activation of glycolysis and the Warburg effect. Our study provides new insights into how CcO regulatory subunits influence cellular metabolic networks and radioresistance in GBM under hypoxia, identifying potential therapeutic targets for improved treatment strategies.
    Keywords:  COX4–1; Cytochrome c oxidase; Glioma; Hypoxia; Mitochondrial supercomplexes; Radioresistance
    DOI:  https://doi.org/10.29011/2574-710x.10299
  17. J Biol Chem. 2025 Sep 16. pii: S0021-9258(25)02585-2. [Epub ahead of print] 110733
      Deoxynucleotides (dNTPs) in post-mitotic tissues rely on deoxynucleoside salvage pathways in order to repair and replicate nuclear and mitochondrial DNA (mtDNA). Previous work from our laboratory showed in perfused rat heart and isolated mitochondria that the only substrate for TTP synthesis is thymidine. When thymidylate (TMP) is provided to bypass thymidine kinase 2 (TK2) the substrate is readily dephosphorylated to thymidine before salvage occurs suggesting compartmentalization within the heart mitochondrial matrix. The goal of this work extends these findings in the heart to mitochondria from other post-mitotic tissues, including rat liver, kidney, and brain. Using AZT to block mitochondrial thymidine kinase 2, we demonstrate that TMP cannot serve as a precursor for TTP synthesis in isolated mitochondria from any of these tissues unless it is de-phosphorylated to thymidine first. Broken mitochondria incubated with labeled TMP showed similar results as intact mitochondria, suggesting the findings are not related to TMP transport across the inner mitochondrial membrane. Further, using proximity labeling with immunofluorescence microscopy we provide evidence supporting the hypothesis that TMP compartmentation is accounted for by the interaction of TK2 and CMPK2 in the mitochondria. Differential fraction experiments provide additional evidence that association with TK2 allows CMPK2 to display TMPK2 activity. Together, the results indicate that a two-step phosphorylation of thymidine to TDP occurs because the proximity of TK2 and CMPK2 in the mitochondria prevents TMP from diffusing from the two enzymes.
    Keywords:  cytidine monophosphate kinase 2; mitochondrial disease; mitochondrial metabolism; nucleoside/nucleotide biosynthesis; nucleoside/nucleotide metabolism; thymidine kinase 2
    DOI:  https://doi.org/10.1016/j.jbc.2025.110733
  18. Med Oncol. 2025 Sep 19. 42(11): 479
      The FLT3 internal tandem duplication (FLT3-ITD) mutation is a critical molecular marker in acute myeloid leukemia (AML) and is closely associated with adverse patient prognosis. Although FLT3 inhibitors have been clinically applied, their therapeutic efficacy is constrained by reduced drug responsiveness and disease relapse. This study aims to investigate the underlying causes of the limited therapeutic efficacy of FLT3 inhibitors in FLT3-ITD-positive AML cells and propose feasible solutions. We screened datasets associated with Gilteritinib and Quizartinib in the Gene Expression Omnibus (GEO) database for enrichment analysis and validated potential key pathways that may limit their therapeutic efficacy through qPCR and Western blot. By assessing proliferation, apoptosis, and cell cycle in MV4-11 and MOLM-13 cells, we verified the combined effects of the ERK1/2 inhibitor Ulixertinib with Gilteritinib or Quizartinib, and further explored the underlying mechanisms via transcriptome sequencing. Gilteritinib and Quizartinib both significantly activated the RAS/MAPK pathway in FLT3-ITD-positive AML cells. While the ERK1/2 inhibitor Ulixertinib alone did not inhibit FLT3-ITD-positive AML cells viability, its combination with Gilteritinib or Quizartinib exhibited potent synergistic effects. Transcriptome sequencing revealed that these synergistic effects may stem from the regulation of gene expression such as PKD1, NR2E3, KDF1, and PRSS8 as well as modulation of ion channel activity. This in vitro study identifies aberrant activation of the RAS/MAPK pathway as a critical factor limiting the efficacy of FLT3 inhibitors in FLT3-ITD-positive AML and demonstrates the potent synergistic effects of Ulixertinib combined with FLT3 inhibitors in FLT3-ITD-positive AML cells, providing a novel therapeutic strategy for AML.
    Keywords:  Acute myeloid leukemia (AML); ERK1/2 inhibitor; FLT3 inhibitor; FLT3 internal tandem duplication (FLT3-ITD); RAS/MAPK pathway
    DOI:  https://doi.org/10.1007/s12032-025-03054-z
  19. bioRxiv. 2025 Sep 05. pii: 2025.09.05.674553. [Epub ahead of print]
      Genetically encoded DNA recorders convert transient biological events into stable genomic mutations, offering a means to reconstruct past cellular states. However, current approaches to log historical events by modifying genomic DNA have limited capacity to record the magnitude of biological signals within individual cells. Here, we introduce MitoScribe, a mitochondrial DNA (mtDNA)-based recording platform that uses mtDNA base editors (DdCBEs) to write graded biological signals into mtDNA as neutral, single-nucleotide substitutions at a defined site. Taking advantage of the hundreds to thousands of mitochondrial genome copies per cell, we demonstrate MitoScribe enables reproducible, highly sensitive, non-destructive, durable, and high-throughput measurements of molecular signals, including hypoxia, NF-κB activity, BMP and Wnt signaling. We show multiple modes of operation, including multiplexed recordings of two independent signals, and coincidence detection of temporally overlapping signals. Coupling MitoScribe with single-cell RNA sequencing and mitochondrial transcript enrichment, we further reconstruct signaling dynamics at the single-cell transcriptome level. Applying this approach during the directed differentiation of human induced pluripotent stem cells (iPSCs) toward mesoderm, we show that early heterogeneity in response to a differentiation cue predicts the later cell state. Together, MitoScribe provides a scalable platform for high-resolution molecular recording in complex cellular contexts.
    DOI:  https://doi.org/10.1101/2025.09.05.674553
  20. Pflugers Arch. 2025 Sep 20.
      Single-nucleotide polymorphisms in mitochondrial DNA (mtDNA) encoded genes of respiratory chain complexes are known to be associated with severe diseases and life-threatening syndromes. In the assembly of the ATP synthase, the enzyme that in the final steps of oxidative phosphorylation generates ATP from ADP and inorganic phosphate, two subunits (ATP6 and ATP8) are mtDNA-encoded. In our study, we investigated the impact of a single-nucleotide polymorphism in MT-ATP8 with respect to memory function in a preclinical model. Here, we have employed two conplastic mouse strains. The mouse strain C57BL/6 J-mtAKR/J served as a control with wild-type sequence in MT-ATP8, while C57BL/6 J-mtFVB/NJ exhibited an m.7778G > T transversion. Using two age groups (3 months and 24 months), levels of reactive oxygen species (ROS), spatial learning in the Morris-Water-Maze, and long-term potentiation were assessed. Immunohistologically, the expressions of NeuN and GFAP were quantified. Additionally, the lifespan of both strains was registered. In comparison to young C57BL/6 J-mtFVB/NJ mice, aged animals had higher ROS levels in the hippocampus. A decreased NeuN/GFAP level was found in C57BL/6 J-mtFVB/NJ mice as well as in old animals of the control strain. Aged animals performed worse in the swimming trials, but no significant differences between both strains were detected. The long-term potentiation recordings revealed reduced synaptic plasticity in young C57BL/6 J-mtFVB/NJ mice. Interestingly, C57BL/6 J-mtFVB/NJ mice presented an extended lifespan compared to animals of the control strain. Together, our data suggest a minor impact of a single-nucleotide polymorphism in MT-ATP8 on spatial learning and oxidative stress depending on the neuronal tissue. In line with the concept of mitohormesis, our findings may be linked to the longevity of mice harbouring single-nucleotide polymorphisms.
    Keywords:  ATP synthase; Ageing; Cognition; Conplastic mouse strains; Lifespan; Long-term potentiation; MT-ATP8; MtDNA variants; Oxidative stress; Single-nucleotide polymorphism
    DOI:  https://doi.org/10.1007/s00424-025-03123-2
  21. J Chem Inf Model. 2025 Sep 18.
      Energy coupling processes in respiratory complex I, a large redox-driven proton pump in the inner mitochondrial membrane, remain one of the most enigmatic problems in modern bioenergetics. Recent high-resolution cryo-EM structures of complex I revealed extensive hydration in the interior of the protein, including the buried E channel, which is an acidic charged conduit that bridges the quinone binding cavity with the extended membrane domain of the enzyme. Despite the general agreement that E channel participates in proton transfer, the absence of proton density in the cryo-EM maps poses a significant challenge to develop viable models of proton pumping. By adhering to the hypothesis that E channel catalyzes transfer of proton(s) from the quinone binding cavity to the membrane-bound proton pumping site(s), we performed hybrid quantum mechanics/molecular mechanics (QM/MM) molecular dynamics (MD) simulations using the ∼2.4 Å cryo-EM structure of mitochondrial complex I fromMus musculus. By combining classical atomistic MD simulations with hybrid QM/MM free energy calculations, we identify several energetically favorable Grotthuss-competent proton transfer paths in the E channel region. As part of the long-range coupling in complex I, our calculations show that protonation of a single acidic amino acid residue in the distal MM surroundings can alter the dynamics of proton transfer in the E channel region. Additionally, we pinpoint the gating function of a highly conserved tyrosine residue in the E channel, which undergoes conformational flipping to establish an energetically favorable proton transfer path. In the context of the redox-coupled proton pumping mechanism of complex I, we propose a stepping-stone model of proton transfer through the E channel.
    DOI:  https://doi.org/10.1021/acs.jcim.5c01365
  22. Cell Rep. 2025 Sep 12. pii: S2211-1247(25)01017-4. [Epub ahead of print]44(9): 116246
      We developed the AVID (ATP visualization in vivo directly) mouse, a genetically encoded biosensor mouse enabling real-time, multiscale imaging of ATP dynamics across the whole body, organs, and cellular compartments in living animals. AVID revealed previously undetectable localized ATP depletion near the central vein of the liver after myocardial infarction, spatially linked to kynurenic acid accumulation-a phenomenon invisible to conventional bulk metabolomics. By seamlessly integrating macroscopic organ-level imaging with microscopic spatial metabolomics, AVID establishes a new framework for spatial systems metabolism. Beyond myocardial infarction, this platform offers broad applicability to study organ-organ metabolic communication, spatial metabolic heterogeneity, and localized metabolic shifts across diverse physiological and pathological contexts, providing a transformative resource for metabolic research.
    Keywords:  ATP dynamics; CP: Metabolism; FRET; GO-ATeam biosensor; disease progression; energy metabolism; in vivo imaging; multiscale imaging; myocardial infarction; organ-organ interaction; spatial systems metabolism
    DOI:  https://doi.org/10.1016/j.celrep.2025.116246
  23. Sci Adv. 2025 Sep 19. 11(38): eadw9095
      Cellular iron levels must be tightly regulated to ensure sufficient iron for essential enzymatic functions while avoiding the harmful generation of toxic species. Here, to better understand how iron levels are controlled, we carry out genome-wide mutagenesis screens in human cells. Alongside mapping known components of iron sensing, we determine the relative contributions of iron uptake, iron recycling, ferritin breakdown, and mitochondrial flux in controlling the labile iron pool. We also identify SETD2, a histone methyltransferase, as a chromatin modifying enzyme that controls intracellular iron availability through ferritin breakdown. Functionally, we show that SETD2 inhibition or cancer-associated SETD2 mutations render cells iron deficient, thereby driving resistance to ferroptosis and potentially explaining how some tumors evade antitumoral immunity.
    DOI:  https://doi.org/10.1126/sciadv.adw9095
  24. Heart. 2025 Sep 16. pii: heartjnl-2025-326082. [Epub ahead of print]
       BACKGROUND: The impact of ketone supplementation, low carbohydrate diets (LCDs) and ketogenic diets (KDs) on heart failure (HF) outcomes is largely unknown. This systematic review and meta-analysis investigated how these dietary changes impacted cardiac function and HF outcomes.
    METHOD: A systematic search of MEDLINE, Embase, CINAHL and Web of Science was performed; last search on 19 November 2025. Randomised controlled trials (RCTs) and observational studies in humans receiving ketone supplementation, LCD and KD interventions were included. Studies were eligible if they reported at least one cardiac function/HF measure. Risk of bias was performed using RoB2 and ROBINS-I (Risk Of Bias In Non-randomised Studies of Interventions). Treatment effects were pooled, mean differences and 95% CIs calculated. Subgroup analysis was performed and heterogeneity was assessed.
    RESULTS: 14 studies were included in this systematic review. A meta-analysis was performed on six RCTs. Ketone supplementation increased left ventricular ejection fraction by 3.12% (95% CI 0.95% to 5.30%, p<0.01), with greater improvement in patients with HF with reduced ejection fraction (HFrEF); 4.25% (95% CI 1.99% to 6.51%, p<0.001). In patients with HFrEF, ketone supplementation increased peak systolic annular velocity (0.60% (95% CI 0.17% to 1.02%, p<0.01)) and cardiac output (1.24 L/min (95% CI 0.24 to 2.24, p<0.05)), compared with controls. Due to small cohorts and different treatment durations, assessment of certainty was low to high. Meta-analysis could not be performed on LCD or KD studies, due to low study numbers.
    CONCLUSIONS: Ketone supplementation significantly improved cardiac function compared with controls, especially in people with HFrEF. More research is needed to determine how low carbohydrate and ketogenic diets affect HF outcomes.
    PROSPERO REGISTRATION NUMBER: CRD42024615367.
    Keywords:  Echocardiography; Heart Failure; Heart Failure, Diastolic; Heart Failure, Systolic; Meta-Analysis
    DOI:  https://doi.org/10.1136/heartjnl-2025-326082