摘要
目的:研究溶血磷脂酸(LPA)对宫颈癌HeLa细胞增殖、黏附、迁移和凋亡的影响及其作用机制。方法:LPA作用于细胞后,细胞计数法观察细胞的增殖;MTT法测定细胞对顺铂的敏感性、流式细胞仪检测顺铂诱导的凋亡;tran-swell小室检测细胞迁移能力变化;黏附实验测定细胞黏附力;同时,观察抑制剂Y27632、LY294002、PD98059对LPA功能的影响。结果:LPA以时间和剂量依赖方式促进细胞增殖,MEK1抑制剂显著抑制LPA的促增殖作用;LPA以剂量依赖方式显著促进HeLa细胞的迁移、和对细胞外基质的黏附,Rho激酶抑制剂显著抑制LPA诱导的迁移和黏附;LPA保护顺铂诱导的细胞凋亡,PI3K抑制剂可显著阻止LPA此作用。结论:LPA可以通过多种信号传导通路途径促进宫颈癌细胞的增殖、迁移和黏附,并抑制细胞凋亡。
AIM: To observe the effect of lysophosphatidic acid on cervical cancer cell line HeLa cells proliferation, adhesion, migration and apoptosis and study related signaling pathway. METHODS: After HeLa cells affected by LPA, the level of proliferation was drawing grouth curve ater cell couting; the sensitivity to cisplatin was evaluated by methyl thiazolyl tetrazolium (MTT) assay and flow cytometry was used to examine cell apoptosis; the potentiality of migration was evaluated by transwell chamber, then to observe the effect of Y27632, LY294002 and PD08059 on biological function of LPA. RESULTS: LPA could promote HeLa cell proliferate on time-dependent and dose-dependent relationship. MEK1 inhibitor could inhibite LPA-induced cell proliferation; LPA promoted the adhesion and migrationof HeLa cells in dose-dependence; Rho inhibitor could inhibit the LPA-induced adhesion and migration; LPA could reduce the chemotherapy sensibility of cervical cancer to DDP in dose-dependence, then PI3K inhibitor could resist this effect. CONCLUSION: LPA could promote HeLa cells'proliferation, adhesion, migration and anti-apoptotosis through multiple signaling pathways.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2009年第8期702-705,共4页
Chinese Journal of Cellular and Molecular Immunology
关键词
宫颈癌
LPA
增殖
黏附
凋亡
信号通路
cervical carcinoma
LPA
proliferation
adhesion
apoptosis
signaling pathway