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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。
AIM: To investigate whether triptorelin inhibits the proliferation of ovarian cancer OVCAR3 cells while reversing cisplatin resistance and exploring the mechanism of MAP-ERK1 / 2 and its regulation. Methods: To establish a cisplatin-resistant subunit cell line OVCAR3-DDP. MTT, flow cytometry and Western blot were used to compare the cell growth of OVCAR3-DDP cells treated with cisplatin, triptorelin and two drugs at different concentrations The ERK1 / 2 protein expression was measured. Results: The drug resistance index of ovarian cancer OVCAR3-DDP cells was 3.87; the sensitivity of cisplatin and triptorelin combined chemotherapy was 2.23; the activity of ERK1 / 2 protein was increased in cisplatin-treated group; in triptorelin- Cisplatin and triptorelin combined treatment group decreased. Conclusion: Triptorelin increases the sensitivity of ovarian cancer OVCAR3-DDP cells to cisplatin, which may be related to the intracellular ERK1 / 2 signal transduction pathway.