bims-medica Biomed News
on Metabolism and diet in cancer
Issue of 2025–03–02
thirteen papers selected by
Brett Chrest, Wake Forest University



  1. bioRxiv. 2025 Feb 13. pii: 2025.02.10.637542. [Epub ahead of print]
      Obesity is an established risk factor for breast cancer (BC), yet the specific mechanisms driving this association remain unclear. Dysregulated lipid metabolism has emerged as a key factor in cancer cell biology. While obesity is often accompanied by hyperlipidemia, the isolated impact of elevated lipid levels on BC growth has not been experimentally tested. Using the E0771 orthotopic model of obesity-accelerated BC growth in immune-competent mice, we investigated the direct role of systemic lipids in tumor growth. Combining dietary and genetic mouse models, we show that elevated circulating lipids are sufficient to accelerate BC tumor growth even in the absence of obesity or alterations in blood glucose and/or insulin levels. Pharmacological lowering of systemic lipid levels attenuates BC growth in obese mice, suggesting a direct role for lipids in fueling tumor expansion. Notably, we also show that weight loss alone, without a corresponding reduction in lipid levels such as that induced by a ketogenic diet, fails to protect against BC, highlighting the necessity of targeting lipid metabolism in obesity-associated BC. Our findings establish hyperlipidemia as a critical driver of BC progression and suggest that lipid-lowering interventions may be a promising strategy to mitigate BC risk in obese individuals.
    DOI:  https://doi.org/10.1101/2025.02.10.637542
  2. ACS Bio Med Chem Au. 2025 Feb 19. 5(1): 184-193
      Malonyl-CoA is the essential building block of fatty acids and regulates cell function through protein malonylation and allosteric regulation of signaling networks. Accordingly, the production and use of malonyl-CoA is finely tuned by the cellular energy status. Most studies of malonyl-CoA dynamics rely on bulk approaches that take only a snapshot of the average metabolic state of a population of cells, missing out on heterogeneous differences in malonyl-CoA and fatty acid biosynthesis that could be occurring among a cell population. To overcome this limitation, we have developed a genetically encoded fluorescent protein-based biosensor for malonyl-CoA that can be used to capture malonyl-CoA dynamics in single cells. This biosensor, termed Malibu (malonyl-CoA intracellular biosensor to understand dynamics), exhibits an excitation-ratiometric change in response to malonyl-CoA binding. We first used Malibu to monitor malonyl-CoA dynamics during inhibition of fatty acid biosynthesis using cerulenin in Escherichia coli, observing an increase in Malibu response in a time- and dose-dependent manner. In HeLa cells, we used Malibu to monitor the impact of fatty acid biosynthesis inhibition on malonyl-CoA dynamics in single cells, finding that two inhibitors of fatty acid biosynthesis, cerulenin and orlistat, which inhibit different steps of fatty acid biosynthesis, increase malonyl-CoA levels. Altogether, we have developed a new genetically encoded biosensor for malonyl-CoA, which can be used to study malonyl-CoA dynamics in single cells, providing an unparalleled view into fatty acid biosynthesis.
    DOI:  https://doi.org/10.1021/acsbiomedchemau.4c00103
  3. J Nutr Biochem. 2025 Feb 20. pii: S0955-2863(25)00036-1. [Epub ahead of print] 109873
       INTRODUCTION: Brown adipose tissue (BAT) exhibits greater resilience against inflammation compared to white adipose tissue. However, chronic consumption of a high-fat diet can render brown adipocytes vulnerable to pro-inflammatory conditions, leading to a decline in their thermogenic capacity and subsequent dysfunction. The analysis of the effects of type fatty acids intake must be important in the context of the dietary pattern and obesity.
    OBJECTIVES: This study aims to investigate the impact of a low-carbohydrate/high-fat diet, enriched with different types of fatty acids, on mitochondrial activity on brown adipose tissue in obese mice.
    METHODS: Male mice were allocated into different dietary groups: a control diet (CTL), and a high-fat diet (HFD) for a duration of 10 weeks to induce obesity. Subsequently, the HFD group was subdivided into the following categories for an additional 6 weeks: HFD with a low carbohydrate content enriched with saturated fatty acids; HFD with a low carbohydrate content enriched with fish oil; HFD with a low carbohydrate content enriched with soybean oil; and HFD with a low carbohydrate content enriched with olive oil.
    RESULTS: The findings indicated that in comparison to a low-carbohydrate diet rich in saturated fats, diets rich in unsaturated fatty acids-particularly omega-6 (n-6) and omega-9 (n-9)-resulted in elevated expression of UCP1, a marker of BAT activity. Moreover, there was an increase in the expression of PGC1-α, a protein involved in mitochondrial biogenesis, and enhanced functionality of the oxidative phosphorylation system within BAT mitochondria. These results suggest that n-6 and n-9 fatty acids may confer greater benefits to BAT functionality than saturated fats within the context of a low-carbohydrate diet. Therefore, this study revealed some molecular components that mediate BAT mitochondria function influenced by different fatty acids in a low carbohydrate diet, making it an important therapeutic target in obesity.
    Keywords:  Adipose tissue; fatty acids; low-carbohydrate diet; mitochondrial complex; obesity
    DOI:  https://doi.org/10.1016/j.jnutbio.2025.109873
  4. Cancer Metab. 2025 Feb 25. 13(1): 11
       INTRODUCTION: Triple-negative breast cancer (TNBC), which tends to be more advanced when diagnosed and more aggressive than other breast cancer subtypes, is accelerated by obesity. Hypertrophic adipocytes and cancer cells exhibit increased oxidative stress and altered redox homeostasis, influencing therapeutic outcomes. Enzymes implicated in both redox regulation and TNBC include glutathione peroxidase 4 (GPX4; reduces lipid peroxides) and pyruvate carboxylase (PC; essential in oxidative stress protection). Using preclinical models, we characterized interactions between GPX4, PC, and oxidative stress in TNBC cells, and established effects of GPX4 suppression on TNBC progression. In TNBC cells, PC knockdown increased GPX4 expression, while GPX4 knockdown increased PC expression. GPX4 inhibition by erastin or RSL3 enhanced TNBC cell death in vitro, and antioxidants mitigated the cytotoxicity. In obese mice, GPX4 knockdown, versus scramble control: (i) reduced tumor burden following orthotopic transplantation of TNBC cells; and (ii) reduced lung metastasis following tail vein injection of TNBC cells in combination with chemotherapy (carboplatin) but not immunotherapy (anti-CTLA4 plus anti-PD1). We conclude that GPX4 and PC expression are inversely related in TNBC cells, and GPX4 and obesity interact to impact TNBC progression and treatment responses. Moreover, GPX4-mediated redox defense, alone or in combination with chemotherapy, is a targetable vulnerability for treating TNBC, including obesity-related TNBC.
    IMPLICATION: GPX4 suppression, alone or with current TNBC therapies, impacts outcomes in preclinical TNBC models with or without obesity and offers a new, plausible mechanistic target for TNBC treatment.
    DOI:  https://doi.org/10.1186/s40170-025-00380-8
  5. Life (Basel). 2025 Jan 23. pii: 160. [Epub ahead of print]15(2):
      The available literature reports inconclusive findings regarding the frequency of organic food consumption and cancer incidence. This systematic review evaluated the effect of the frequency of organic food consumption on overall and site-specific cancer risk. Four electronic databases (PubMed, Scopus, Web of Science Core Collection, and Embase), the gray literature, and the reference lists of the included reports were searched for eligible studies. Study screening, data abstraction, and risk of bias assessment were performed by two independent examiners. Hazard ratios (HRs) and 95% confidence intervals using a random effects model were utilized to synthesize the available data from the included studies. There was no difference between the two interventions regarding overall cancer (HR = 0.93, 95% CI: 0.78-1.12), breast cancer (HR = 1.01, 95% CI: 0.81-1.26), colorectal cancer (HR = 1.01, 95% CI: 0.93-1.10), and non-Hodgkin lymphoma risks (HR = 0.70, 95% CI: 0.17-2.94). The findings suggest that the overall and site-specific cancer risk are not associated with the frequency of consumption of organic foods. Further research is necessary to provide more evidence for the role of organic food consumption on the incidence of cancer using homogeneous methodologies to define the frequency of organic food consumption.
    Keywords:  frequency; organic food; systematic review; tumor
    DOI:  https://doi.org/10.3390/life15020160
  6. Neoplasia. 2025 Feb 24. pii: S1476-5586(25)00022-3. [Epub ahead of print]62 101143
      Resistance to mitochondrial apoptosis is a major driver of chemoresistance in pancreatic ductal adenocarcinoma (PDAC). However, pharmacological manipulation of the mitochondrial apoptosis threshold in PDAC cells remains an unmet therapeutic goal. We hypothesized that fatty acid synthase inhibitors (FASNis), a family of targeted metabolic therapeutics recently entering the clinic, could lower the apoptotic threshold in chemoresistant PDAC cells and be synergistic with BH3 mimetics that neutralize anti-apoptotic proteins. Computational studies with TVB-3166 and TVB-3664, two analogues of the clinical-grade FASNi TVB-2640 (denifanstat), confirmed their uncompetitive behavior towards NADPH when bound to the FASN ketoacyl reductase domain. The extent of NADPH accumulation, a consequence of FASN inhibition, paralleled the sensitivity of PDAC cells to the apoptotic effects of TVB FASNis in conventional PDAC cell lines that naturally express varying levels of FASN. FASN inhibition dramatically increased the sensitivity of "FASN-high" expressing PDAC cells to the BCL2/BCL-XL/BCL-W inhibitor ABT-263/navitoclax and the BCL2-selective inhibitor ABT-199/venetoclax, both in vitro and in in vivo xenografted tumors. The ability of TVB FASNis to shift the balance of pro- and anti-apoptotic proteins and thereby push PDAC cells closer to the apoptotic threshold was also observed in cell lines developed from patient-derived xenografts (PDXs) representative of the classical (pancreatic) transcriptomic subtype of PDAC. Experiments in PDAC PDXs in vivo confirmed the synergistic antitumor activity of TVB-3664 with navitoclax and venetoclax, independent of the nature of the replication stress signature of patient-derived PDAC cells. The discovery that targeted inhibition of FASN is a metabolic perturbation that sensitizes PDAC cells to BH3 mimetics warrants further investigation to overcome resistance to mitochondrial apoptosis in PDAC patients.
    Keywords:  BH3 mimetics; Fatty acid synthase; Gemcitabine; Pancreatic cancer
    DOI:  https://doi.org/10.1016/j.neo.2025.101143
  7. Lipids Health Dis. 2025 Feb 27. 24(1): 76
       BACKGROUND: Cardiolipin (CL) is a signature phospholipid of mitochondria that maintains the integrity of mitochondrial membrane and supports proper mitochondrial function. Alterations in CL level and composition can impair or, conversely, improve mitochondrial function and bioenergetics, both of which are critical for cancer metabolism. However, conflicting reports on CL levels across different cancer types and limited research using human patient samples limit our understanding of its diagnostic potential.
    METHODS: This cross-sectional study explores CL concentrations in gastric and colon cancer tissues using a CL-specific fluorescent probe MitoCLue and compares them to adjacent healthy tissues.
    RESULTS: In gastric cancer, CL levels showed no significant differences between tumor and healthy tissues, suggesting that metabolic shifts in gastric cancer do not affect total CL content. In contrast, colon cancer tissues exhibited a significant 33% increase in CL levels, indicating mitochondrial adaptation and/or increase in mitochondrial mass in colon cancer. No associations were found between CL levels and patient demographic factors; although a weak correlation with body mass index was noted.
    CONCLUSION: We successfully applied MitoCLue to quantitatively assess the total CL level in healthy and tumor tissues from patients with gastric or colon cancer. The distinct CL levels in gastric and colon cancer suggest that there are cancer-type specific mitochondrial adaptations, reflecting unique bioenergetic demands and metabolic reprogramming pathways. While a 33% increase in CL levels was observed in colon cancer tissues compared to healthy adjacent tissues, this modest variation may limit its utility as a standalone biomarker.
    Keywords:  Biomarker; Cardiolipin; Colon cancer; Diagnostic; Gastric cancer
    DOI:  https://doi.org/10.1186/s12944-025-02499-5
  8. Adv Nanobiomed Res. 2024 Dec;pii: 2400107. [Epub ahead of print]4(12):
      The Glioblastoma (GBM) tumor microenvironment is heterogeneous, complex, and is being increasingly understood as a significant contributor to tumor progression. In brain tumors, the extracellular matrix contains a large concentration of Hyaluronic acid (HA) that makes it important to study its role in cancer progression. In particular, abnormal accumulation of HA is observed in gliomas and is often associated with poor prognosis. In addition, HA is a polymer and its molecular weight (MW) distribution may influence tumor cell activity. Here, we evaluate the influence of the molecular weight of HA on tumor cell metabolism. We use a 2D cell culture approach to expose the U87-MG cell line to different HA MWs (10, 60, and 500 kDa) and glucose concentrations (0, 5.5, and 25 mM). Notably, we found that HA influences GBM amino acid metabolism via reduction in LAT1 transporter protein expression. We also report an influence on mitochondrial respiration levels and a difference in the accumulation of some key products of cell metabolic activity (lactic acid, glutamic acid and succinic acid). Overall, these results indicate that HA MW can influence GBM metabolic state, with implications for cell invasion and tumor progression.
    Keywords:  Hyaluronic acid; amino acid; glioblastoma; glucose; metabolism; molecular weight
    DOI:  https://doi.org/10.1002/anbr.202400107
  9. Mol Oncol. 2025 Feb 24.
      Glioblastoma (GB) is the most aggressive primary brain tumor with poor prognosis despite multimodal therapy. Calorie-restricted diets have emerged as putative strategies to augment anticancer therapies. We employed UHPLC-high-resolution mass spectrometry analyses of plasma lipids and polar metabolites to assess the systemic metabolic effects of a 72-h preoperative fasting period in IDH-wild-type glioma patients (n = 9 GB and n = 1 diffuse pediatric-type high-grade H3/IDH-wildtype) who participated in the prospective ERGO3 trial (NCT04461938). Fasting reduced lysophosphatidylcholines (LPC, LPC-O), lysophosphatidylethanolamines (LPE, LPE-O), and increased free fatty acids and carnitines. Triglyceride (TG) profiles shifted from short-chain TGs (42-48 C-atoms) to very long-chain TGs (58-60 C-atoms) indicating an exploitation of neutral lipid stores. Branched-chain amino acids, aminobutyric acid, and uric acids were increased, and glucose reduced after fasting. The effects of fasting were comparable in men and women. To our knowledge, this is the first study that evaluated the effects of fasting on systemic lipid/metabolite levels in GB patients. Our results may hold promise for integrating fasting interventions as a component of a potential metabolic tumor therapy.
    Keywords:  fasting; glioblastoma; lipidomic; lysophosphatidylcholines; metabolomic; plasma
    DOI:  https://doi.org/10.1002/1878-0261.70003
  10. bioRxiv. 2025 Feb 11. pii: 2025.02.10.635159. [Epub ahead of print]
       Introduction: The survival rate for children and adolescents has increased to over 85%. However, there is limited understanding of the impact of pediatric cancers on muscle development and physiology. Given that brain tumors alone account for 26% of all pediatric cancers, this study aimed to investigate the skeletal muscle consequences of tumor growth in young mice.
    Methods: C2C12 myotubes were co-cultured with GL261 murine glioblastoma cells to assess myotube size. GL261 cells were then injected subcutaneously into 4-week-old male C57BL/6J mice. Animals were euthanized 28 days post-GL261 implantation. Muscle function was tested in vivo and ex vivo . Muscle protein synthesis was measured via the SUnSET method, and gene/protein expression levels were assessed via Western blotting and qPCR.
    Results: In vitro , the C2C12 cultures exposed to GL261 exhibited myotube atrophy, consistent with a disrupted anabolic/catabolic balance. In vivo , carcass, heart, and fat mass were significantly reduced in the tumor-bearing mice. Skeletal muscle growth was impeded in the GL261 hosts, along with smaller muscle CSA. Both in vivo muscle torque and the ex vivo EDL muscle force were unchanged. At molecular level, the tumor hosts displayed reduced muscle protein synthesis and increased muscle protein ubiquitination, in disagreement with decreased muscle ubiquitin ligase mRNA expression.
    Conclusions: Overall, we showed that GL261 tumors impact the growth of pediatric mice by stunting skeletal muscle development, decreasing muscle mass, reducing muscle fiber size, diminishing muscle protein synthesis, and altering protein catabolism signaling.
    DOI:  https://doi.org/10.1101/2025.02.10.635159
  11. J Biol Chem. 2025 Feb 25. pii: S0021-9258(25)00198-X. [Epub ahead of print] 108349
      Glioblastoma (GBM) is a highly aggressive primary malignant adult brain tumor that inevitably recurs with a fatal prognosis. This is due in part to metabolic reprogramming that allows tumors to evade treatment. Therefore, we must uncover the pathways mediating these adaptations to develop novel and effective treatments. We searched for genes that are essential in GBM cells as measured by a whole-genome pan-cancer CRISPR screen available from DepMap and identified the methionine metabolism genes MAT2A and AHCY. We conducted genetic knockdown, evaluated mitochondrial respiration, and performed targeted metabolomics to study the function of these genes in GBM. We demonstrate that MAT2A or AHCY knockdown induces oxidative stress, hinders cellular respiration, and reduces the survival of GBM cells. Furthermore, selective MAT2a or AHCY inhibition reduces GBM cell viability, impairs oxidative metabolism, and shifts the cellular metabolic profile towards oxidative stress and cell death. Mechanistically, MAT2a and AHCY regulate spare respiratory capacity, the redox buffer cystathionine, lipid and amino acid metabolism, and prevent oxidative damage in GBM cells. Our results point to the methionine metabolic pathway as a novel vulnerability point in GBM. Significance We demonstrated that methionine metabolism maintains antioxidant production to facilitate pro-tumorigenic ROS signaling and GBM tumor cell survival. Importantly, targeting this pathway in GBM has the potential to reduce tumor growth and improve survival in patients.
    Keywords:  glioblastoma; lipid peroxidation; metabolism; metabolomics; methionine; mitochondria; oxidative stress
    DOI:  https://doi.org/10.1016/j.jbc.2025.108349
  12. Methods Mol Biol. 2025 ;2882 47-79
      5'-Adenosine monophosphate-activated protein kinase (AMPK) senses cellular metabolic status and reflects the balance between ATP production and ATP usage. This balance varies from cell to cell and changes over time, creating a need for methods that can capture cellular heterogeneity and temporal dynamics. Fluorescent biosensors for AMPK activity offer a unique approach to measure metabolic status nondestructively in single cells in real time. In this chapter, we provide a brief rationale for using live-cell biosensors to measure AMPK activity, survey the current AMPK biosensors, and discuss considerations for using this approach. We provide methodology for introducing AMPK biosensors into a cell line of choice, setting up experiments for live-cell fluorescent microscopy of AMPK activity, and calibrating the biosensors using immunoblot data.
    Keywords:  AMPKAR; Biosensors; Fluorescent protein reporters; Forster resonance energy transfer (FRET); Live-cell microscopy; Metabolic signaling; Single cell
    DOI:  https://doi.org/10.1007/978-1-0716-4284-9_3
  13. mBio. 2025 Feb 25. e0379824
      Guanosine triphosphate (GTP) is essential for macromolecular biosynthesis, and its intracellular levels are tightly regulated in bacteria. Loss of the alarmone (p)ppGpp disrupts GTP regulation in Bacillus subtilis, causing cell death in the presence of exogenous guanosine and underscoring the critical importance of GTP homeostasis. To investigate the basis of guanosine toxicity, we performed a genetic selection for spontaneous mutations that suppress this effect, uncovering an unexpected link between GTP synthesis and glycolysis. In particular, we identified suppressor mutations in pyk, which encodes pyruvate kinase, a glycolytic enzyme. Metabolomic analysis revealed that inactivating pyruvate kinase prevents guanosine toxicity by reducing GTP levels. Although traditionally associated with ATP generation via substrate-level phosphorylation, B. subtilis pyruvate kinase in vitro was found to produce GTP and UTP approximately 10 and three times more efficiently than ATP, respectively. This efficient GTP/UTP synthesis extends to Enterococcus faecalis and Listeria monocytogenes, challenging the conventional understanding of pyruvate kinase's primary role in ATP production. These findings support a model in which glycolysis directly contributes to GTP synthesis, fueling energy-demanding processes, such as protein translation. Finally, we observed a synergistic essentiality of the Δndk Δpyk double mutant specifically on glucose, indicating that pyruvate kinase and nucleoside diphosphate kinase are the major contributors to nucleoside triphosphate production and complement each other during glycolysis. Our work highlights the critical role of nucleotide selectivity in pyruvate kinase and its broader implications in cellular physiology.
    IMPORTANCE: In this study, we reveal that pyruvate kinase, a key glycolytic enzyme, primarily generates GTP from GDP in Bacillus subtilis, relative to other nucleotide triphosphates, such as ATP. This finding, uncovered through genetic selection for mutants that suppress toxic GTP overaccumulation, challenges the conventional understanding that pyruvate kinase predominantly produces ATP via substrate-level phosphorylation. The substantial role of GTP production by pyruvate kinase suggests a model where glycolysis rapidly and directly supplies GTP as the energy currency to power high GTP-demanding processes such as protein synthesis. Our results underscore the importance of nucleotide selectivity (ATP vs GTP vs UTP) in shaping the physiological state and fate of the cell, prompting further exploration into the mechanisms and broader implications of this selective nucleotide synthesis.
    Keywords:  (p)ppGpp; GTP; glycolysis; nucleotide metabolism; pyruvate kinase
    DOI:  https://doi.org/10.1128/mbio.03798-24