ArticleTranslational cancer research2025
Glutamine metabolism drives tumor aggressiveness but not chemoresistance in ovarian carcinoma cell lines.
Article in Translational cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Glutamine metabolism in ovarian carcinoma: disentangling tumor aggressiveness from chemoresistance.Translational cancer research · 2026Article
- Unraveling glutamine metabolism in ovarian carcinoma: signaling cross-talk, positron emission tomography utility, and therapeutic boundaries.Translational cancer research · 2026Article
- Immune heterogeneity and therapeutic resistance in gynecological malignancies.Frontiers in immunology · 2026Review
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9 authors.
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Abstract
Background: Glutamine, an essential nutrient for healthy cells, supports immunity and cytoprotection during anticancer treatments. However, intense glutaminolysis may promote proliferation and chemoresistance in ovarian carcinomas by activating the PI3K/AKT/mTORC1 pathway and overexpressing c-Myc. This study aimed to characterize glutamine metabolism in ovarian carcinomas and assess its impact on tumor aggressiveness and chemosensitivity, to inform nutritional supplementation or therapeutic targeting. Methods: Glutamine and glucose consumption, chemosensitivity to cisplatin and paclitaxel, and doubling time were analyzed in three ovarian carcinoma cell lines (ES-2, TOV-21G: clear cell; OVCAR-3: serous papillary) and primary ascites cells under varying glutamine concentrations (0.5, 1, 2, 4 mM). Expression of glutaminase, glutamate dehydrogenase 1 (GDH1), and c-Myc, as well as PI3K/AKT/mTORC1 activation, were assessed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Results: TOV-21G exhibited significantly higher glutamine consumption (13.3±1.3 Conclusions: Intense glutaminolysis is associated with increased tumor aggressiveness, suggesting a prognostic role for
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