氯喹促进顺铂诱导胃癌SGC7901细胞凋亡及其机制

  目的  研究自噬对顺铂（cisplatin，DDP）诱导的胃癌SGC7901细胞凋亡的影响，并初步探讨其可能机制。  方法  DDP和（或）氯喹处理胃癌SGC7901细胞，MTT法检测细胞增殖，流式细胞术检测细胞凋亡，MDC染色后荧光显微镜观察自噬囊泡，West. ern Blot检测自噬和凋亡相关蛋白。  结果  5 mg/L的顺铂作用于胃癌SGC7901细胞24 h，细胞凋亡率为21.07%±2.12%，同时观测到自噬囊泡增多和LC3-Ⅱ蛋白表达升高；氯喹特异性抑制自噬活性后，提高了顺铂诱导的细胞凋亡率（30.16%±3.54%，P < 0.05）；检测到凋亡相关蛋白Caspase-3和P53表达增加，Bcl-2蛋白表达下降。  结论  自噬在顺铂诱导胃癌SGC7901细胞凋亡的过程中起保护作用，氯喹抑制自噬后，可能通过激活P53蛋白及灭活Bcl-2蛋白的表达来促进细胞凋亡，联合应用顺铂和氯喹有望成为胃癌治疗的新策略。 

Chloroquine promotes DDP-induced apoptosis in human gastric cancer cell line SGC7901

  Objective  To investigate the mechanism and effects of autophagy on cisplatin(DDP)-induced apoptosis in human gastric cancer cell line SGC7901.   Methods  Cell proliferation was determined by an MTT assay after the SGC7901 cells were treated with DDP and/or chloroquine. Cell apoptosis was determined by flow cytometry. Autophagy and related protein expressions were detected by Western blot. Autophagy was quantitatively analyzed by fluorescence microscopy after monodansylcadaverine staining was performed.   Results  The cells were treated with 5 mg/L of DDP for 24 h, the rate of cell apoptosis was (21.07 ± 2.12)%. Autophagy, characterized by an increase in the number of autophagic vesicles and LC3-II protein level, was observed in DDP-treated cells. After autophagy was inhibited by chloroquine, the rate of cell apoptosis was increased to (30.16 ± 3.54)%. In addition, caspase-3 and P53 protein levels were increased, but Bcl-2 protein was decreased.   Conclusion  Autophagy protected human gastric cancer cell line SGC7901 from DDP-induced apoptosis. In addition, the inhibition of autophagy could promote apoptosis. The combined therapy of DDP and chloroquine may be a promising therapeutic strategy for gastric cancer.