中文摘要：

目的探讨膀胱癌细胞中着色性干皮病C组基因（xeroderma pigmentosum group C,XPC）蛋白缺失对自噬的影响。方法利用shRNA策略,建立稳定干扰XPC的膀胱癌T24细胞模型,蛋白印迹技术检测干扰XPC后自噬表征蛋白LC3Ⅱ的表达,瞬时转染GFP-LC3,荧光显微镜观察细胞荧光聚集情况,CCK-8法检测细胞的增殖状况,免疫印迹技术检测自噬及凋亡相关蛋白的表达。结果成功建立干扰XPC的膀胱癌T24细胞模型;干扰XPC后,膀胱癌T24细胞自噬小体的形成[（1.53±0.81）%vs（3.30±0.70）%,P〈0.05]明显减少,顺铂作用下膀胱癌T24细胞自噬小体的形成[（2.19±0.37）%vs（3.20±0.29）%,P〈0.05]明显减少;顺铂促进XPC缺失后的膀胱癌T24细胞自噬;XPC缺失后的自噬为非保护性自噬。结论 XPC蛋白参与调控膀胱癌T24细胞的自噬。

英文摘要：

Objective To determine the effect of deficiency of xeroderma pigmentosum group C（ XPC） on the autophagy in bladder cancer cells. Methods By using shRNA,a stable XPC deficient cell model was established based on human bladder cancer T24 cells. The protein level of LC3 Ⅱ was detected by Western blotting to monitor the autophagy. GFP-LC3 puncta were visualized by using fluorescence microscopy after transiently transfected with a GFP-LC3 expression vector. Cell viability was detected by CCK-8 assay.The expression of the proteins involved in apoptosis and autophagy signaling was detected by Western blot assay. Results A stable XPC deficient model of T24 cells was successfully established. Knocking down of XPC resulted in decreases of autophagosome formation under both normal [（ 1. 53 ± 0. 81） % vs（ 3. 30 ±0. 70） %,P 0. 05] and cisplatin-induced DNA damage condition [（ 2. 19 ± 0. 37） % vs（ 3. 20 ± 0. 29） %,P 0. 05]. Cisplatin promoted cell autophagy in XPC deficient T24 cells. Autophagy played a non-protective role in XPC deficient cells when dealing with cisplatin induced DNA damage. Conclusion XPC is involved in the autophagy in T24 cells.