ArticleScientific reports2025
Metformin combined with CB-839 specifically inhibits KRAS-mutant ovarian cancer.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Overcoming Therapy Resistance in Ovarian Cancer: From Molecular Mechanisms to Emerging Therapeutic Strategies.Cancers · 2026Review
- Targeted therapeutic strategies forTranslational lung cancer research · 2026Review
- Dependency of Non-Small Cell Lung Cancer Cells on Glutamine and Glucose Levels in the Presence of Metformin.The Eurasian journal of medicine · 2026Article
- Precision oncology in gynecologic cancers: molecular taxonomy, biomarker-guided therapeutics, and the challenge of therapeutic resistance.Frontiers in oncology · 2026Review
- Glutamine Metabolism: Role in Cancer Cell Proliferation and Survival.Cancer treatment and research · 2026Review
- Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025Review
- Ammonia metabolism and ammonia-induced cell death: role in cancer therapy.Cell communication and signaling : CCS · 2025Review
- Glutaminase Expression in Canine Large-Cell Alimentary Lymphoma Cells and Effects of Glutaminase Inhibition by CB-839.Veterinary medicine and science · 2025Article
- Targeting glutamine metabolism as a potential target for cancer treatment.Journal of experimental & clinical cancer research : CR · 2025Review
- Radio-chemotherapy and metformin selectively modulate the heterogeneous landscape of glioma with ribosome biogenesis, long non coding RNA and immune-escape markers as major player.International journal of biological sciences · 2025Article
- Research progress on FOXM1 in ovarian cancer diagnosis and therapeutics.Frontiers in oncology · 2025Review
- Metabolic Reprogramming Shapes the Progression and Therapeutic Landscape of Ovarian Cancer.Cancer management and research · 2025Review
- Glutamine metabolism and ammonia death: targeted modulation for enhanced cancer immunotherapy.Frontiers in immunology · 2025Review
- Endoplasmic reticulum stress orchestrates tumor metabolism and immunity: new insights into immunometabolic therapeutics.Frontiers in immunology · 2025Review
- Microbiota-host metabolism reprogramming in colorectal cancer: from pathogenesis to precision therapies.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
KRAS mutations can cause metabolic reprogramming in ovarian cancer, leading to an increased metastatic capacity. This study investigated the metabolic reprogramming changes induced by KRAS mutations in ovarian cancer and the mechanism of action of metformin combined with a glutaminase 1 inhibitor (CB-839). KRAS-mutant ovarian cancer accounted for 14% of ovarian cancers. The expression of glucose metabolism-related (PFKFB3, HK2, GLUT1, and PDK2) and glutamine metabolism-related enzymes (GLS1 and ASCT2) was elevated in KRAS-mutant ovarian cancer cells compared with that in wild-type cells. KRAS-mutant cells had a higher aerobic oxidative capacity than did wild-type cells. Metformin inhibited proliferation, the expression of glucose metabolism-related enzymes, and the aerobic oxidative capacity of KRAS-mutant cells compared with those of control cells. Furthermore, it enhanced the expression of glutamine metabolism-related enzymes in KRAS-mutant cells. Metformin combined with CB-839 inhibited the proliferation and aerobic oxidation of KRAS-mutant cells to a greater extent than that observed in wild-type cells. Additionally, the inhibitory effects of metformin and CB-839 in the KRAS-mutant ovarian cancer NOD-SCID mouse model were significantly stronger than those in the drug-alone group. KRAS mutations lead to enhanced glucose and glutamine metabolism in ovarian cancer cells, which was inhibited by metformin combined with CB-839.
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