bFGF对卵巢癌CAOV3细胞Bcl-2、Bcl-xl、Bax、Bad表达的影响

目的研究bFGF调控卵巢癌CAOV3凋亡的信号通路及对Bcl-2、Bcl-xl、Bax、Bad表达的影响。方法无血清饥饿诱导细胞凋亡。分为饥饿对照、bFGF、bFGF PD98059、bFGF Wortmannin组。流式细胞术、DNA Ladder检测细胞凋亡;Western印迹法检测ERK、PKB、Bad活性以及Bcl-2、Bax表达,RT- PCR检测Bcl-2、Bcl-xl mRNA变化。结果bFGF促进p-ERK、p-PKB、p-Bad、Bcl-2表达,抑制Bax表达及饥饿诱导的细胞凋亡。激酶抑制剂PD98059可抑制bFGF对ERK、Bcl-2、Bax的调节作用,Wortmannin可抑制bFGF对PKB、Bad、Bax的调控作用,二者均可阻断bFGF对凋亡的抑制作用。bFGF对Bcl-xl表达无影响。结论bFGF可能通过激活MEK/ERK、P13K/PKB信号途径通路调节Bcl-2、Bax、Bad表达,抑制饥饿诱导的卵巢癌CAOV3细胞凋亡。

Effects of bFGF on the Expressions of Bcl-2,Bcl-xl,Bax and Bad in Ovarian Cancer CAOV3 Cells

Objective To investigate the effects of bFGF on the expression of Bcl-2,Bcl-xl, Bad and Bax and to explore its anti-apoptotic mechanism by MEK/ERK,PI3K/PKB signal trans- duction pathway in ovarian cancer cell line CAOV3.Methods Cell apoptosis was induced by star- vation.After treatment with bFGF,PD98059 and Wortmannin,FACScan flow cytometry and DNA Ladder were used to detect apoptosis.ERK,PKB,Bad,Bcl-2 and Bax were determined by Western blotting and RT-PCR was performed to observe Bcl-2 and Bcl-xl mRNA.Results bFGF inhibited the cell apoptosis and upregulated the expressions of p-ERK,p-PKB,p-Bad and Bcl-2,but inhibi- ted Bax.PD9809 inhibited the effects of bFGF on ERK,Bel-2 and Bax.Wortmannin inhibited its regulatory effects on PKB,Bad and Bax.They all inhibited its effects on apoptosis.Conclusion Bcl-2,Bax and Bad might prevent cell apoptosis via MEK/ERK and PI3K/PKB signal transduction pathway activated by bFGF in CAOV3 cell line.