bims-glucam Biomed News
on Glutamine cancer metabolism
Issue of 2024–10–20
eleven papers selected by
Sreeparna Banerjee, Middle East Technical University



  1. EMBO J. 2024 Oct 17.
      Triple-negative breast cancer (TNBC) metabolism and cell growth uniquely rely on glutamine uptake by the transporter ASCT2. Despite previous data reporting cell growth inhibition after ASCT2 knockdown, we here show that ASCT2 CRISPR knockout is tolerated by TNBC cell lines. Despite the loss of a glutamine transporter and low rate of glutamine uptake, intracellular glutamine steady-state levels were increased in ASCT2 knockout compared to control cells. Proteomics analysis revealed upregulation of macropinocytosis, reduction in glutamine efflux and increased glutamine synthesis in ASCT2 knockout cells. Deletion of ASCT2 in the TNBC cell line HCC1806 induced a strong increase in macropinocytosis across five ASCT2 knockout clones, compared to a modest increase in ASCT2 knockdown. In contrast, ASCT2 knockout impaired cell proliferation in the non-macropinocytic HCC1569 breast cancer cells. These data identify macropinocytosis as a critical secondary glutamine acquisition pathway in TNBC and a novel resistance mechanism to strategies targeting glutamine uptake alone. Despite this adaptation, TNBC cells continue to rely on glutamine metabolism for their growth, providing a rationale for targeting of more downstream glutamine metabolism components.
    Keywords:  ASCT2; Glutamine Metabolism; Macropinocytosis; Metabolomics; Triple-Negative Breast Cancer
    DOI:  https://doi.org/10.1038/s44318-024-00271-6
  2. J Neuroinflammation. 2024 Oct 15. 21(1): 261
      The NLR family pyrin domain containing 3 (NLRP3) inflammasome in microglia is intimately linked to the pathogenesis of Alzheimer's disease (AD). Although NLRP3 inflammasome activity is regulated by cellular metabolism, the underlying mechanism remains elusive. Here, we found that under the pathological conditions of AD, the activation of NLRP3 inflammasome in microglia is accompanied by increased glutamine metabolism. Suppression of glutaminase, the rate limiting enzyme in glutamine metabolism, attenuated the NLRP3 inflammasome activation both in the microglia of AD mice and cultured inflammatory microglia. Mechanistically, inhibiting glutaminase blocked the anaplerotic flux of glutamine to the tricarboxylic acid cycle and amino acid synthesis, down-regulated mTORC1 signaling by phosphorylating AMPK, which stimulated mitophagy and limited the accumulation of intracellular reactive oxygen species, ultimately prevented the activation of NLRP3 inflammasomes in activated microglia during AD. Taken together, our findings suggest that glutamine metabolism regulates the activation of NLRP3 inflammasome through mitophagy in microglia, thus providing a potential therapeutic target for AD treatment.
    Keywords:  Alzheimer’s disease; Glutamine metabolism; Microglia; Mitophagy; NLRP3 inflammasome
    DOI:  https://doi.org/10.1186/s12974-024-03254-w
  3. J Clin Invest. 2024 Oct 01. pii: e177242. [Epub ahead of print]
      Females have an increased prevalence of many Th17 cell-mediated diseases, including asthma. Androgen signaling decreases Th17 cell-mediated airway inflammation, and Th17 cells rely on glutaminolysis. However, it remains unclear whether androgen receptor (AR) signaling modifies glutamine metabolism to suppress Th17 cell-mediated airway inflammation. We show that Th17 cells from male humans and mice had decreased glutaminolysis compared to females, and that AR signaling attenuated Th17 cell mitochondrial respiration and glutaminolysis in mice. Using allergen-induced airway inflammation mouse models, we determined females had a selective reliance upon glutaminolysis for Th17-mediated airway inflammation, and AR signaling attenuated glutamine uptake in CD4+ T cells by reducing expression of glutamine transporters. Minimal reliance on glutamine uptake in male Th17 cells compared to female Th17 cells was also found in circulating T cells from patients with asthma. AR signaling thus attenuates glutaminolysis, demonstrating sex-specific metabolic regulation of Th17 cells with implications for Th17 or glutaminolysis targeted therapeutics.
    Keywords:  Asthma; Immunology; Pulmonology; Sex hormones; T cells
    DOI:  https://doi.org/10.1172/JCI177242
  4. bioRxiv. 2024 Oct 11. pii: 2024.10.10.617667. [Epub ahead of print]
      Restricting amino acids from tumors is an emerging therapeutic strategy with significant promise. While typically considered an intracellular antioxidant with tumor-promoting capabilities, glutathione (GSH) is a tripeptide of cysteine, glutamate, and glycine that can be catabolized, yielding amino acids. The extent to which GSH-derived amino acids are essential to cancers is unclear. Here, we find that GSH catabolism promotes tumor growth. We show that depletion of intracellular GSH does not perturb tumor growth, and extracellular GSH is highly abundant in the tumor microenvironment, highlighting the potential importance of GSH outside of tumors. We find supplementation with GSH can rescue cancer cell survival and growth in cystine-deficient conditions, and this rescue is dependent on the catabolic activity of γ-glutamyltransferases (GGTs). Finally, pharmacologic targeting of GGTs' activity prevents the breakdown of circulating GSH, lowers tumor cysteine levels, and slows tumor growth. Our findings indicate a non-canonical role for GSH in supporting tumors by acting as a reservoir of amino acids. Depriving tumors of extracellular GSH or inhibiting its breakdown is potentially a therapeutically tractable approach for patients with cancer. Further, these findings change our view of GSH and how amino acids, including cysteine, are supplied to cells.
    DOI:  https://doi.org/10.1101/2024.10.10.617667
  5. Int J Gynecol Cancer. 2024 Oct 15. pii: ijgc-2024-005920. [Epub ahead of print]
       OBJECTIVE: Increased glutamine metabolism by cancer cells via upregulation of the drug-targetable enzyme glutaminase may contribute to an immune-suppressive tumor microenvironment. Inhibiting glutamine metabolism can not only suppress tumor growth, but also enhance tumor-specific immunity. We investigated the relationship between glutaminase expression, the immune tumor microenvironment, and clinicopathologic features in endometrial cancer.
    METHODS: Tissue microarrays constructed from 87 primary endometrial cancer specimens were stained by immunohistochemistry for glutaminase, c-Myc, mutL homolog 1 (MLH1), mutS homolog 2 (MSH2), mutS homolog 6 (MSH6), postmeiotic segregation increased 2 (PMS2), estrogen receptor (ER), progresterone receptor (PR), CD8, FoxP3, CD68, programmed cell death protein 1 (PD-1), and programmed cell death ligand 1 (PD-L1). We compared the immune tumor microenvironment and clinicopathologic features between glutaminase-high (H-score≥median) versus glutaminase-low (H-score<median) endometrial cancers. We also evaluated data from The Cancer Genome Atlas (TCGA) for 527 endometrial cancer patients in whom RNA-Seq for glutaminase expression was performed and compared long-term clinical outcomes between glutaminase-high (RNA-Seq Z-score≥median) versus glutaminase-low (RNA-Seq score<median) patients.
    RESULTS: In the tissue microarray analysis, glutaminase expression was positively correlated with c-Myc expression (r=0.4226, p<0.0001). Glutaminase-high endometrial cancers were associated with non-endometrioid histology (p=0.0001), high histologic grade (p=0.0004), myometrial invasion (p=0.017), advanced stage (p=0.012), increased FoxP3+ regulatory T cells (p=0.008), increased CD68+ tumor-associated macrophages (p=0.010), and higher PD-L1 combined positive scores (p=0.043). In the TCGA analysis, glutaminase-high (RNA-Seq Z-score≥median) patients showed worse overall (p=0.004) and progression-free (p=0.032) survival than glutaminase-low (RNA-Seq score<median) patients.
    CONCLUSIONS: Our findings indicate that increased glutaminase expression is associated with an immune-suppressive tumor microenvironment, poor clinicopathologic features, and worse long-term outcomes in patients with endometrial cancer.
    Keywords:  Immunotherapy; Pathology; Uterine Cancer
    DOI:  https://doi.org/10.1136/ijgc-2024-005920
  6. Cell Metab. 2024 Oct 11. pii: S1550-4131(24)00374-7. [Epub ahead of print]
      Despite the known metabolic benefits of exercise, an integrated metabolic understanding of exercise is lacking. Here, we use in vivo steady-state isotope-labeled infusions to quantify fuel flux and oxidation during exercise in fasted, fed, and exhausted female mice, revealing several novel findings. Exercise strongly promoted glucose fluxes from liver glycogen, lactate, and glycerol, distinct from humans. Several organs spared glucose, a process that broke down in exhausted mice despite concomitant hypoglycemia. Proteolysis increased markedly, also divergent from humans. Fatty acid oxidation dominated during fasted exercise. Ketone production and oxidation rose rapidly, seemingly driven by a hepatic bottleneck caused by gluconeogenesis-induced cataplerotic stress. Altered fuel consumption was observed in organs not directly involved in muscle contraction, including the pancreas and brown fat. Several futile cycles surprisingly persisted during exercise, despite their energy cost. In sum, we provide a comprehensive, integrated, holistic, and quantitative accounting of metabolism during exercise in an intact organism.
    Keywords:  TCA cycle; circulating metabolites; energy metabolism; exercise; in vivo flux quantification; isotope tracing; skeletal muscle
    DOI:  https://doi.org/10.1016/j.cmet.2024.09.010
  7. Oncol Rep. 2024 Dec;pii: 167. [Epub ahead of print]52(6):
      Renal cell carcinoma (RCC) is distinguished by its varied metabolic reprogramming driven by tumor suppressor gene dysregulation and oncogene activation. Tumors can adapt nutrient uptake and metabolism pathways to meet the altered biosynthetic, bioenergetic and redox demands of cancer cells, whereas conventional chemotherapeutics and molecular inhibitors predominantly target individual metabolic pathways without addressing this adaptability. Flavonoids, which are well‑known for their antioxidant and anti‑inflammatory properties, offer a unique approach by influencing multiple metabolic targets. The present comprehensive review reveals the intricate processes of RCC metabolic reprogramming, encompassing glycolysis, mitochondrial oxidative phosphorylation and fatty acid biosynthesis. The insights derived from the present review may contribute to the understanding of the specific anticancer mechanisms of flavonoids, potentially paving the way for the development of natural antitumor drugs focused on the metabolic reprogramming of RCC.
    Keywords:  RCC; Warburg effect; anticancer drug; flavonoids; metabolic reprogramming
    DOI:  https://doi.org/10.3892/or.2024.8826
  8. Amino Acids. 2024 Oct 13. 56(1): 60
      The gastrointestinal tract's epithelial barrier plays a crucial role in maintaining health. This study aims to investigate the impact of glutamine supplementation on intestinal permeability, considering its importance for immune function and nutrient absorption. The study adhered to the PRISMA protocol for systematic reviews and meta-analyses. A systematic search was performed in four databases (PubMed, Scopus, Web of Science, and Google Scholar) until April 2023 to identify clinical trials on glutamine supplementation and gastrointestinal permeability. Eligibility criteria included randomized placebo-controlled trials measuring gut permeability post-glutamine supplementation. Studies were included regardless of language or publication date. Data extraction involved study characteristics, intervention details, and outcomes. Quality assessment was performed using the Cochrane tool, and statistical analysis utilized mean differences and standard deviations with a random effects model. Subgroup analysis was conducted to explore heterogeneity. The systematic review and meta-analysis included 10 studies from 1998 to 2014 with 352 participants. A total of 216 patients were enrolled in the intervention group, and 212 in the control group. The mean participant age was 46.52 years. The participants had different types of diseases in terms of their health status. Overall, glutamine supplementation did not significantly affect intestinal permeability (WMD: -0.00, 95% CI -0.04, 0.03). Subgroup analysis showed a significant reduction in intestinal permeability with doses over 30g/day (WMD: -0.01, 95% CI -0.10, -0.08). The glutamine supplements were administered orally in all included studies. The meta-analysis demonstrated a significant reduction in intestinal permeability with glutamine supplementation exceeding 30 mg/day for durations of less than 2 weeks. Further investigations with varying dosages and patient populations are warranted to enhance understanding and recommendations regarding glutamine supplementation's effects on gut permeability.
    Keywords:  Glutamine; Intestinal permeability; Meta-analysis; Supplement
    DOI:  https://doi.org/10.1007/s00726-024-03420-7
  9. J Hazard Mater. 2024 Oct 09. pii: S0304-3894(24)02672-4. [Epub ahead of print]480 136093
      Hexavalent chromium [Cr(VI)] exposure increases the risk of cancer occurrence. This study found that the levels of an atypical methyltransferase, METTL16 were greatly upregulated in the cells, and mouse tissues with Cr(VI) exposure, and played a critical role in cell proliferation and tumor growth induced by Cr(VI). Similarly, we found METTL16 was upregulated in various human cancer tissues. To understand mechanism of METTL16 in inducing carcinogenesis and cancer development, we identified that glutamate-ammonia ligase (GLUL) as the METTL16 functional target for regulating glutamine metabolism and tumorigenesis induced by Cr(VI) exposure. We demonstrated that METTL16 promoted GLUL expression in a m6A-dependent manner. Furthermore, METTL16 methylated the specific stem-loop structure of GLUL transcript, thereby increased the recognition and splicing of pre-GLUL RNA modified site by m6A reader YTHDC1, which ultimately accelerated the production of mature GLUL mRNA. Animal model of Cr(VI) exposure further confirmed that the expression levels of METTL16 and GLUL were both significantly induced in vivo, and there had a significant positive correlation between METTL16 and GLUL levels. Furthermore, we found that YTHDC1 was also important in inducing GLUL expression, and MYC was the upstream mediator of METTL16 to increase its transcriptional activation. Our study revealed new mechanism of metal carcinogenesis and cancer development.
    Keywords:  Cancer development; Carcinogenesis; Cr(VI); GLUL; METTL16
    DOI:  https://doi.org/10.1016/j.jhazmat.2024.136093
  10. Heliyon. 2024 Oct 15. 10(19): e38718
      Cancer growth requires high amount of nicotinamide adenine dinucleotide phosphate (NADPH) to feed the anabolic reactions and preserve the redox balance. NADPH level is largely preserved by the oxidative arm of the pentose phosphate pathway (PPP). Here, we show that prolonged glucose deprivation of triple negative breast cancer MDA-MB-231 cells decreases proliferation rate, promotes hexose funneling to glycolysis hampering the PPP. The impairment in PPP activity and the consequent NADPH depletion are partially counterbalanced by enhancing the malic enzyme-1 catalyzed conversion of glutamine-derived malate to pyruvate. However, the use of these glucose-independent carbons implies the integrity of the two PPPs represented in all eukaryotic cells, i.e., the well-recognized cytosolic PPP, triggered by glucose-6-phosphate dehydrogenase (G6PD) and its reticular counterpart, triggered by hexose-6P-dehydrogenase (H6PD). This evidence configures the reticular PPP as a mandatory player in the regeneration of NADPH reductive power by cancer cells.
    Keywords:  G6PD; Glucose metabolism; H6PD; NADPH; Pentose phosphate pathway; Redox stress; Triple negative breast cancer
    DOI:  https://doi.org/10.1016/j.heliyon.2024.e38718
  11. Exp Eye Res. 2024 Oct 11. pii: S0014-4835(24)00346-4. [Epub ahead of print] 110124
      Diabetic mellitus causes various complications, including the corneal endothelial dysfunction (CED) that leads to corneal edema and vision loss, especially in the DM patients with intraocular surgeries. However, the pathogenic mechanism of hyperglycemia-caused CED remains incomplete understood. Here we firstly screened and identified the glutamine contents of anterior humor were significantly reduced in both the type 2 diabetic patients and streptozotocin-induced type 1 diabetic mice. To explore the potential therapeutic effects of glutamine supplement on the protection of diabetic corneal endothelial dysfunction, we performed the anterior chamber perfusion with the addition of L-alanyl-L-glutamine (Ala-Gln), and confirmed that Ala-Gln supplement not only accelerated the resolution of corneal edema and recovery of corneal thickness, but also preserved the regular arrangement and barrier-pomp function of corneal. Mechanistically, we revealed that the supplements of Ala-Gln protect corneal endothelial cells from the deleterious effects of high glucose-induced oxidative stress, mitochondrial dysfunction, and cell apoptosis. Overall, these results indicate the glutamine depletion plays an important role in the diabetic corneal endothelial dysfunction, while the Ala-Gln supplement during intraocular surgery provide an effective prevention strategy through regulating the redox homeostasis and mitochondrial function of corneal endothelial cells.
    Keywords:  Diabetes; corneal endothelium; glutamine; mitochondria; oxidative stress
    DOI:  https://doi.org/10.1016/j.exer.2024.110124