ArticleMolecular oncology2024
Targeting metabolic reprogramming to overcome drug resistance in advanced bladder cancer: insights from gemcitabine- and cisplatin-resistant models.
Article in Molecular oncology, 2024. 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.
- FASN Promotes Malignant Progression of Bladder Cancer by Regulating Lipid Metabolism via the ERK/PPAR Pathway.Cell biochemistry and biophysics · 2026Article
- Single-cell and spatial transcriptomics identify CAPG as a key driver of cisplatin resistance in bladder cancer.Functional & integrative genomics · 2026Article
- The controversial role of metabolic reprogramming in anti-tumor therapy resistance.Discover oncology · 2026Review
- Hypoxia-inducible factor 1α exerts dual roles in bladder cancer progression through TIMP3-mediated regulation of angiogenesis and invasion.Scientific reports · 2026Article
- From molecular networks to translational intervention: current progress in the mechanisms of gemcitabine resistance in bladder cancer.Frontiers in immunology · 2026Review
- The emerging role of ZDHHC9 in cancer: from protein palmitoylation to tumor progression and immune regulation.Frontiers in immunology · 2026Review
- A systematic characterization of amino acid metabolism-related genes reveals molecular subtypes and a prognostic signature in bladder cancer.Frontiers in oncology · 2026Article
- Derazantinib enhances gemcitabine efficacy in PDAC by attenuating the NF-κB and MAPK pathways to suppress MUC5AC expression.Medical oncology (Northwood, London, England) · 2025Article
- Curcumol overcomes cisplatin resistance and rewires glycolysis-H3K9la-ORC6 axis to trigger ferroptosis in bladder cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- Cytoskeletal protein KRT14 governs cisplatin resistance by modulating eIF4H-dependent ACOX2 translation and lipid metabolism in bladder cancer.Cell death & disease · 2025Article
- Article
- Dioscin initiates dual roles in bladder cancer progression via miR-195-5p/FASN/SLC3A2 axis-mediated cell death mechanisms.Translational oncology · 2025Article
- Long non-coding RNA MINCR silencing contributes to suppressed gemcitabine resistance in bladder cancer by blocking the ZEB1/PHGDH axis through microRNA-876-5p up-regulation.Journal of molecular histology · 2025Article
- Article
- Ferroptosis in Cancer: Mechanism and Therapeutic Potential.International journal of molecular sciences · 2025Review
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Authors and funding
15 authors.
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Abstract
Gemcitabine plus cisplatin (GC) combination chemotherapy is the primary treatment for advanced bladder cancer (BC) with unresectable or metastatic disease. However, most cases develop resistance to this therapy. We investigated whether drug resistance could be targeted through metabolic reprogramming therapies. Metabolomics analyses in our lab's gemcitabine- and cisplatin-resistant cell lines revealed increased phosphoglycerate dehydrogenase (PHGDH) expression in gemcitabine-resistant cells compared with parental cells. Isocitrate dehydrogenase 2 (IDH2) gain of function stabilized hypoxia-inducible factor1α (HIF1α) expression, stimulating aerobic glycolysis. In gemcitabine-resistant cells, elevated fumaric acid suppressed prolyl hydroxylase domain-containing protein 2/Egl nine homolog 1 (PHD2) and stabilized HIF1α expression. PHGDH downregulation or inhibition in gemcitabine-resistant BC cells inhibited their proliferation, migration, and invasion. Cisplatin-resistant cells showed elevated fatty acid metabolism, upregulating fatty acid synthase (FASN) downstream of tyrosine kinase. Using the fibroblast growth factor receptor (FGFR) tyrosine kinase inhibitor erdafitinib, we inhibited malonyl-CoA production, which is crucial for fatty acid synthesis, and thereby suppressed upregulated HIF1α expression. Combination treatment with NCT503 and erdafitinib synergistically suppressed tumor cell proliferation and induced apoptosis in vitro and in vivo. Understanding these mechanisms could enable innovative BC therapeutic strategies to be developed.
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