曲谱瑞林逆转卵巢癌OVCAR-3细胞对顺铂的耐药性分析

Triptorelin Reverses the Resistant of Human Ovarian Carcinoma Cells (OVCAR-3) to Cisplatin via MAPK-ERK1/2 Signal Pathway

目的:研究曲普瑞林能否逆转卵巢癌OVCAR3细胞对顺铂的耐药性,并探讨其调节机制。方法:采用MTT、流式细胞技术以及Western印迹方法比较不同浓度顺铂、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蛋白的表达情况。结果:顺铂与曲普瑞林联合其化疗增敏倍数为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,而且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 cisplatinresistant OVCAR-3 ovarian carcinoma cell line in vitro. Methods：After treated respectively with cisplatin, triporelin, and combination （cisplatin and triptorelin） in different concentration, the proliferation, cycle, apoptosis and ERK1/2 activation of OVCAR3-DDP cells were detected by MTT assay, flow cytometry and Western blotting, respectively. Results： The reversal reaction （RR） induced by combination was 2.23; ERK1/2 activation in OVCAR3-DDP ceils was up regulated by cisplatin, but was down regulated by triptorelin and combination. Conclusion：Triptorelin can increase the cytotoxic effects of cisplatin on OVCAR3-DDP cells in vitro by modulating the activity of the MAPK-ERK1/2 signaling pathway.