The Therapeutic Effects of M4 to Ovarian Cancer Cell Lines and the Primary Mechanism
|School||Huazhong University of Science and Technology|
|Course||Obstetrics and Gynaecology|
|Keywords||STAT3 Select Copy adenovirus M4 Gene therapy OV2008 C13K|
[Objective] To study explore its preliminary mechanism of the OV2008 and C13K ovarian cancer cell lines in vitro treatment effect , and select Copy adenovirus M4 . 【Methods】 replication adenovirus M4 , infected ovarian cancer cell lines OV2008 and C13K MTT method detection M4 inhibition of proliferation of ovarian cancer cell lines ; flow cytometric detection M4 apoptosis ; Western Blot detection changes in expression of STAT3 protein and its downstream target proteins ; flow cytometry to detect cell cycle ; the Transwell assay M4 of invasive ability of two ovarian cancer cell lines . DDP role in ovarian cancer resistant strain C13K MTT detect cell proliferation simultaneously by flow cytometry to detect apoptosis . M4 with the combined effects of DDP C13K MTT to detect cell proliferation changes ; expression of MDR-1 Western Blot detection cells . 【Results】 choose the replication of adenovirus M4 significantly inhibited the OV2008 , and C13K cell proliferation ( P <0.05 ) , but also to promote the two cell apoptosis ( P <0.05 ) , p- STAT3 after infection M4 Western Blot , STAT3 protein and target protein Bcl -xl , survivin , Cyclin D1 expression level decreased significantly ( P <0.05 ) ; the Transwell law results show that the M4 can inhibit ovarian cancer cell invasion ability ( P <0.05 ) . Low concentrations of cisplatin for C13K significantly induce apoptosis ( P gt; 0.05 ) , nor its proliferation inhibition significantly ( P gt ; 0.05) . Acting on M4 and DDP C13K significantly inhibited cell proliferation ( P lt; 0.05 ) , MDR-1 expression in the cells significantly down-regulated ( P lt; 0.05 ) . [Conclusion] select the replication of adenovirus M4 good treatment effect on ovarian cancer cell lines in vitro , but also able to reverse of C13K to cisplatin resistance , the mechanism may be due to the M4 closed STAT3 gene in the tumor cells , thereby promoting the p - STAT3, survivin , Bcl-xl , Cyclin D1 , MMP -9 expression levels decreased at the same time C13K MDR-1 significantly down , eventually leading to apoptosis of tumor cells .