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目的探讨细胞外信号激酶(ERK)在紫杉醇引起的卵巢癌细胞调亡中的作用。方法用紫杉醇处理人卵巢上皮性腺癌细胞株Caov-3 and Skov-3,应用二氨基联苯染色,在显微镜下观察其凋亡。应用蛋白印迹法技术,用特异性识别双磷酸化ERK1/2的抗体,检测卵巢癌细胞经泰素作用后ERK1/2的活化情况。用MTT法检测PD98059对泰素引导的卵巢癌细胞毒性的影响。结果在80 nM泰素导致Caov-3 和Skov3细胞凋亡和ERK1/2激活,泰素作用9 h后,出现ERK的激活,15 h后活性最大。用100μM 的PD 98059 作用于不同药物浓度(60 nM 和80 nM)的泰素作用的细胞,细胞存活率显著降低(P <0.05)。结论泰素能激活卵巢癌Caov-3 和Skov3细胞ERK。抑制ERK的活性能提高Caov-3 和Skov3细胞对泰素的敏感性。阻断MEK1/ERK信号转导通路,可以增加泰素对卵巢癌的细胞毒作用。
Objective To investigate the role of extracellular signal kinase (ERK) in paclitaxel-induced ovarian cancer cell apoptosis. Methods Paclitaxel was used to treat human ovarian epithelial adenocarcinoma cell line Caov-3 and Skov-3, and its apoptosis was observed under microscope. Western blotting was used to detect the activation of ERK1 / 2 with paclitaxel in ovarian cancer cells by using an antibody specifically recognizing bisphosphorylated ERK1 / 2. The effect of PD98059 on the cytotoxicity of Taxol-induced ovarian cancer cells was detected by MTT assay. Results The apoptosis of Caov-3 and Skov3 cells induced by 80 nM taxol and the activation of ERK1 / 2 were observed. After 9 h of taxol treatment, ERK activation was observed and the activity was maximal after 15 h. Cells treated with docetaxel at different drug concentrations (60 nM and 80 nM) with 100 μM PD 98059 significantly reduced cell viability (P <0.05). Conclusion Taxol activates ERK in ovarian cancer cells Caov-3 and Skov3. Inhibition of ERK activity can increase the sensitivity of Taxol to Caov-3 and Skov3 cells. Blocking the MEK1 / ERK signal transduction pathway can increase the cytotoxic effect of taxol on ovarian cancer.