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目的:探讨抑制ClC-3基因表达对顺铂(DDP)复制的人卵巢癌SKOV3/DDP细胞损伤促进作用过程中的具体作用机制,为应用DDP治疗卵巢癌提供实验依据。方法:转染pSH1-siRNA-ClC-3重组质粒到人卵巢癌SKOV3/DDP细胞,Western blotting方法观察热休克蛋白(HSP70)、溶酶体组织蛋白酶D(cathepsin D)蛋白表达。结果:与SKOV3细胞比较,SK-OV3/DDP细胞中HSP70蛋白表达增加(P<0.05)。转染pSH1-siRNA-ClC-3重组质粒联合DDP作用后,SKOV3/DDP细胞中HSP70蛋白表达降低(P<0.05),cathepsin D蛋白表达增加(P<0.05)。结论:抑制ClC-3基因表达促进顺铂诱导SKOV3/DDP细胞凋亡的可能作用机制与溶酶体膜通透性(LMP)增加有关。
OBJECTIVE: To investigate the specific mechanism of action of ClC-3 gene in promoting the injury of human ovarian cancer SKOV3 / DDP cells replicated by cisplatin (DDP), and provide experimental evidence for the application of DDP in the treatment of ovarian cancer. Methods: The recombinant plasmid pSH1-siRNA-ClC-3 was transfected into human ovarian cancer SKOV3 / DDP cells. The expression of heat shock protein 70 (HSP70) and cathepsin D protein were detected by Western blotting. Results: Compared with SKOV3 cells, the expression of HSP70 protein in SK-OV3 / DDP cells increased (P <0.05). After transfected with pSH1-siRNA-ClC-3 recombinant plasmid and DDP, the expression of HSP70 protein in SKOV3 / DDP cells was decreased (P <0.05) and cathepsin D protein expression was increased (P <0.05). Conclusion: The possible mechanism of action of inhibiting ClC-3 gene expression and promoting cisplatin-induced SKOV3 / DDP cell apoptosis is related to the increase of lysosomal membrane permeability (LMP).