中文摘要：

目的探讨微管调节蛋白Stathmin对卵巢癌顺铂耐药细胞C13K增殖和化疗敏感性的影响。方法应用蛋白质印记法检测卵巢癌顺铂敏感性0V2008细胞和耐药性C13K细胞Stathmin表达差异；选择C13K为实验细胞．应用siRNA靶向沉默Stathmin（Stathmin—siRNA组），以未转染细胞为空白对照组，以转染阴性干扰为阴性对照组，利用蛋白质印记法检测siRNA转染效果，MTT法测定转染对细胞增殖和顺铂敏感性的影响，流式细胞仪测定转染对顺铂引起的细胞周期的变化。结果Stathmin在细胞C13K的表达较OV2008的表达明显增加。与空白对照组和阴性对照组相比，Stathmin—siRNA组中Stathmin表达明显降低，C13K细胞的增殖明显抑制，Stathmin—siRNA组顺铂半数致死量IC50[（15．41±1．08）μg／mL]明显降低。Stathmin-siRNA组顺铂诱导的G2／M期（27．48_＋0．76）％明显高于顺铂处理的对照组。结论干扰Stathmin能明显抑制C13K细胞的增殖，增强卵巢癌对顺铂的敏感性，为卵巢癌治疗提供新的前景。

英文摘要：

Objective To explore the role of stathmin on the C 13K cell proliferation and chemosensitivity of cisplatin in ovarian cancer. Methods The stathrnin expression in cisplatin-sensitive OV2008 and resistant C13K cells was detected by western blot. Effective stathmin siRNA was transfected into ovarian cancer C13K cells（Stathmin-siRNA group）. Non-transfected cells were used as blank control and negative siRNA as negative control. Western blot was used to verify the siRNA interference result. MTT was used to measure the cell proliferation and the change of ehemosensitivity to cisplatin. Flow cytornetry was used to detect the change of cisplatin-indueed cell cycle arrest. Results Stathmin expression in C13K cells was higher than that in OV2008 cells. Compared to blank control group and negative control group, Stathmin protein was significantly reduced and the proliferation was significantly inhibited in stathmin-siRNA group, and the IC50 of cisplatin in stathmin-siRNA group [（15.41±1.08） μg/mL] was significantly lower. The cell cycle in G2/M phase induced by eisplatin in stathmin-siRNA group [（27.48±0.76）%] was significantly higher than those in control group. Conclusion Interfering with stathmin can effectively inhibit the proliferation of C13K cell and effectively increase eisplatin ehemosensitivity, and provide new prospects for ovarian cancer treatment.