FAP和Rho家族蛋白在卵巢癌侵袭迁移中的作用

目的：明确FAP是否通过RhoA／ROCK、Racl-GTP通路发挥促增殖、侵袭和迁移作用。方法：用MTT实验，Transwell实验和迁移实验检测FAP、RhoA／ROCK、Racl-GTP对卵巢癌细胞系HO-8910PM的增殖，侵袭和迁移的影响。结果：1、MTT法，迁移和侵袭实验证实用Y-27632抑制RhoA／ROCK途径能够促进卵巢癌细胞的增殖、迁移和侵袭，与FAP联合作用时促进作用增强。2、MTT法，迁移和侵袭实验证实NSC23766抑制Racl途径能够抑制卵巢癌细胞的增殖、迁移和侵袭，与FAP联合作用使FAP的促进作用减弱。结论：l、RhoA／ROCK通路抑制HO一8910PM细胞增殖、迁移和侵袭；Racl-GTP促进H0—8910PM细胞增殖、迁移和侵袭。2、FAP不是通过RhoA／ROCK而是通过Racl—GTP信号通路在HO．8910PM细胞发挥促增殖、迁移和侵袭作用的。

FAP and Rho-GTPases on the Invasion and Metastasis of Ovarian Cancer

Objective： To determine whether the FAP promotes the ability of proliferation, invasion and migration of HO-8901PM cells by the RhoA/ROCK, Racl-GTP enzymes. Methods： by detection of FAP using the transwell assay, MTT assay and migration assay, RhoA / ROCK, Racl-GTP on ovarian cancer cell line HO-8910PM proliferation, invasion and migration. Results： 1, MTT, migration and invasion experiments confirmed with Y-27632 inhibited RhoA / ROCK pathway can promote ovarian cancer cell proliferation, migration and invasion, FAP facilitating role was enhanced when combined with Y-27632. 2, MTT method, migration and invasion experiments confirmed NSC23766 inhibited Racl pathway to inhibit ovarian cancer cell proliferation, migration and invasion, the promoting role of FAP was weakened when combined with NSC23766. Conclusions： 1. RhoA / ROCK pathway inhibition of HO-8910PM cell proliferation, migration and invasion; Rac 1-GTP promote HO-8910PM cell proliferation, migration and invasion.2, not by RhoA/ROCK but Racl-GTP signaling pathway, FAP plays a role in HO-8910PM cells proliferation, migration and invasion.