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Молекулярные механизмы резистентности клеток рака мочевого пузыря RT112/GR к гемцитабину
Бюллетень экспериментальной биологии и медицины. 2026. Т. 182. № 9. С. 242–247.
Gemcitabine, a first-line chemotherapeutic agent for bladder cancer (BC), often loses clinical efficacy due to the development of drug resistance, the underlying mechanisms of which remain poorly understood. In this work, a highly gemcitabine-resistant RT112/GR cell line was obtained by long-term selection. The MTT assay revealed a 9312-fold decrease in gemcitabine sensitivity and moderate resistance to cisplatin (2.60-fold, p < 0.0001). Resistant cells acquired mesenchymal features. RT-PCR revealed upregulation of cytidine deaminase (fold change [FC] = 7.2) and downregulation of deoxycytidine kinase (dCK) (FC = 0.15), indicating impaired gemcitabine metabolism. Resistance was accompanied by activation of antioxidant defense and suppression of ferroptosis. Thus, gemcitabine resistance in RT112/GR cells is driven by intracellular drug metabolic reprogramming and enhanced cell survival mechanisms. These findings are important for understanding and overcoming chemoresistance in BC.
Keywords: ferroptosisферроптозbladder cancerрак мочевого пузыряgemcitabine resistancenucleoside metabolismрезистентность к гемцитабинуметаболизм нуклеозидов
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