川芎嗪联合mTOR抑制剂调控卵巢癌SKOV-3细胞增殖、侵袭迁移的实验研究

目的 研究川芎嗪联合mTOR抑制剂对卵巢癌SKOV-3细胞增殖、侵袭迁移的作用.方法 分别设置对照组、40μmol/L川芎嗪组、5μmol/L雷帕霉素组、40μmol/L川芎嗪联合5μmol/L雷帕霉素组,各组SKOV-3细胞给药后继续培养48 h后,MTT法考察各组SKOV-3细胞的增殖抑制率,Transwell实验...

Experimental study on the regulation of proliferation,invasion and migration of SKOV-3 cells in ovary cancer by Ligustrazine and mTOR inhibitors

Objective To study the effect of ligustrazine combined with mTOR inhibitor on proliferation,invasion and migration of ovarian cancer SKOV-3 cells in ovary cancer.Methods The 4 groups,namely control group,40μmol/L ligustrazine group,5μmol/L rapamycin group and 40μmol/L ligustrazine combined with 5μmol/L rapamycin group,were treated with 40μmol/L ligustrazine,5μmol/L rapamycin and 40μmol/L ligustrazine combined with 5μmol/L rapamycin,respectively.After 48 hours of continuous culture,the proliferation inhibition rate of SKOV-3 cells in each group was determined by MTT assay.The invasive ability of SKOV-3 cells was detected by Transwell test,the migration ability of SKOV-3 cells was detected by scratch test,and the mRNA levels of Bax and Bcl-2 in SKOV-3 cells were detected by real-time PCR.The levels of PI3K,Akt and mTOR in SKOV-3 cells were detected by Western blot,and the cell cycle of SKOV-3 in each group was detected by flow cytometry.Results Compared with control group,ligustrazine group and rapamycin group,the proliferation inhibition rate of SKOV-3 cells in ligustrazine combined with rapamycin group was significantly increased(P<0.05),and the invasive ability and migration ability of SKOV-3 cells were significantly decreased(P<0.05).The level of Bax mRNA in SKOV-3 cells increased significantly(P<0.05),the level of Bcl-2 mRNA decreased significantly(P<0.05),the levels of PI3K,Akt and mTOR decreased significantly(P<0.05),and the level of SKOV-3 cells in G1 phase increased significantly(P<0.05).Conclusion Ligustrazine combined with mTOR inhibitor can significantly inhibit the proliferation,invasion and migration of ovarian cancer SKOV-3 cells,and its mechanism may be related to the regulation of PI3K/Akt/mTOR signaling pathway.