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目的:明确FAP是否通过RhoA/ROCK、Rac1-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、Rac1-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Rac1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:1、RhoA/ROCK通路抑制HO-8910PM细胞增殖、迁移和侵袭;Rac1-GTP促进HO-8910PM细胞增殖、迁移和侵袭。2、FAP不是通过RhoA/ROCK而是通过Rac1-GTP信号通路在HO-8910PM细胞发挥促增殖、迁移和侵袭作用的。
Objective: To clarify whether FAP can promote proliferation, invasion and migration through RhoA / ROCK and Rac1-GTP pathways. Methods: The effects of FAP, RhoA / ROCK and Rac1-GTP on the proliferation, invasion and migration of ovarian cancer cell line HO-8910PM were detected by MTT assay, Transwell assay and migration assay. MTT assay showed that Y-27632 inhibited RhoA / ROCK pathway to promote the proliferation, migration and invasion of ovarian cancer cells, and promoted the combination of FAP and FAP. MTT method, migration and invasion experiments confirmed that NSC23766 inhibition of Rac1 pathway can inhibit the proliferation, migration and invasion of ovarian cancer cells, combined with FAP FAP role in the promotion of weakened. RhoA / ROCK pathway inhibited the proliferation, migration and invasion of HO-8910PM cells; Rac1-GTP promoted the proliferation, migration and invasion of HO-8910PM cells. 2, FAP not through RhoA / ROCK but through the Rac1-GTP signaling pathway in HO-8910PM cells play a role in promoting proliferation, migration and invasion.