中文摘要：

目的：探讨有丝分裂激酶Plk1通过磷酸化修饰PinX1调控宫颈癌HeLa细胞有丝分裂及凋亡的作用。方法：运用酵母双杂交、免疫共沉淀、谷胱甘肽-S转移酶沉降实验了解Plk1与PinX1在体内外是否能够相互结合采用;采用体内外磷酸化实验明确Plk1是否能够磷酸化修饰PinX1;采用免疫荧光染色及流式细胞术检测PinX1磷酸化对HeLa细胞有丝分裂及凋亡的影响。结果：Plk1与PinX1在体内外均能结合;Plk1在体内外均可磷酸化修饰PinX1;过量表达PinX1的非磷酸化突变体能够阻碍HeLa细胞的有丝分裂进程;过量表达PinX1的磷酸化突变体导致细胞凋亡的增加（F=76554.133,P〈0.001）。结论：Plk1与PinX1相互结合并通过磷酸化修饰PinX1阻碍细胞有丝分裂进程及促进细胞凋亡。

英文摘要：

Aim： To investigate the effects of phosphorylation of PinX1 by Plkl on mitosis and apoptosis of cervical cancer HeLa cells. Methods ：Using yeast hybridation assay, co-immunopreeipitation and GST pull-down assay to determine the domain of Plkl and PinX1 binding and interaction in vitro and in vivo. To cheek the phosphorylation of PinX1 by Plkl using in vitro phosphorylation assay. Immunofluorescenee assay and flow cytometry were used to analyze the effect of phos- phorylation of PinX1 on apoptosis and mitosis. Results ： Plkl interacted with PinX1 and could be phosphorylated by PinX1 in vivo and in vitro. Overexpression of phospho-mimicking mutant of PinX1 in Hela ceils resulted in significant mitosis de- lay and apoptosis（27 = 76 554. 133,P 〈 0. 001 ）. Conclusion： Plkl and PinX1 could interacted and the Plkl-mediatedphosphorylation of PinX1 is essential for mitosis and apoptosis in HeLa cells.