ERK1/2在曲普瑞林逆转卵巢癌OVCAR-3细胞顺铂耐药中的作用

Triptorelin reverses the resistant of human ovarian carcinoma cells(OVCAR-3) to cisplatin via MAPK-ERK1/2 signal pathway

目的:研究曲普瑞林在抑制卵巢癌OVCAR3细胞增殖的同时可否逆转顺铂耐药,并探讨MAP-ERK1/2在其中的变化及调节机制。方法:筛选建立耐顺铂的亚细胞系OVCAR3-DDP;采用MTT、流式细胞术及Western blot比较不同浓度下顺铂、曲普瑞林及两药联合对耐药卵巢癌OVCAR3-DDP细胞生长的影响,测定ERK1/2蛋白的表达。结果:卵巢癌OVCAR3-DDP细胞耐药指数为3.87;顺铂与曲普瑞林联合化疗增敏倍数为2.23;ERK1/2蛋白活性在顺铂处理组升高,在曲普瑞林处理组、顺铂与曲普瑞林联合处理组降低。结论:曲普瑞林增加了卵巢癌OVCAR3-DDP细胞对顺铂的敏感性,此作用可能与细胞内ERK1/2信号转导通路有关。

Objective：To determine the effect and mechanism of triptorelin on cisplatin-re- sistance reversal in OVCAR-3 ovarian carcinoma cell line. Methods ：Cisplatin-resistant cell subline OVCAR3-DDP was induced. After treated with cisplatin ,triporelin,and combination of cisplatin and triptorelin in different concentration respectively ,the proliferation, cycle, apoptosis and ERK1/2 ac- tivity of OVCAR3-DDP cells were detected by M＇IT assay,flow cytometry and western blotting,respectively. Results：The resistant index of OVCAR3 -DDP cells was 3.87 ,and the reversal reaction （RR） induced by the combination was 2.23 ;ERK1/2 activity in OVCAR3-DDP cells was up-regu- lated by cisplatin,but was down-regulated by triptorelin and the combination. ComtQsion：Triptore- lin can increase the cytotoxic effects of cisplatin on OVCAR3-DDP cells in vitro by modulating the activity of the MAPK-ERK1/2 signaling pathway.