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目的:探讨TCP1-β在雄激素非依赖性前列腺癌细胞(AIPC)增殖中的作用。方法:选择雄激素依赖性的前列腺癌细胞系LnCap和雄激素非依赖性的前列腺癌细胞系PC3作为模型,用不含酚红的培养基和活性炭吸附过的血清培养LnCap和PC3细胞,检测其对雄激素的依赖性;采用RNA干扰(RNAi)技术抑制PC3-Ad和LnCap细胞的TCP1-β表达,Q-PCR、Western blot方法检测TCP1-β的表达变化;MTT方法检测细胞存活率;流式细胞术检测细胞凋亡情况;并用生物信息学方法探讨可能参与TCP1-β调控AIPC增殖的信号通路。结果:①撤除雄激素后,LnCap细胞增殖受到显著抑制,而PC3细胞增殖未受明显影响;②转染TCP1-β的siRNA后,PC3-Ad和LnCap细胞的TCP1-β表达受到显著抑制(P=0.002,P=0.006);③PC3-Ad的TCP1-β表达受到显著抑制后,细胞的增殖受到抑制(P=0.015),但是细胞没有出现明显凋亡;TCP1-β表达抑制对LnCap细胞的增殖和凋亡都没有产生显著影响;④TCP1-β可能参与了PI3K/Akt信号通路对AIPC增殖的调控作用。结论:TCP1-β过表达可能参与了AIPC细胞的增殖调控。
Objective: To investigate the role of TCP1-β in the proliferation of androgen-independent prostate cancer (AIPC) cells. METHODS: LnCap, an androgen-independent prostate cancer cell line, and PC3, an androgen-independent prostate cancer cell line, were selected as models. LnCap and PC3 cells were cultured in phenol red-free medium and activated charcoal-adsorbed serum, Androgen dependence; TCP1-βexpression was inhibited by RNA interference (RNAi) in PC3-Ad and LnCap cells; the expression of TCP1-β was detected by Q-PCR and Western blot; the cell viability was detected by MTT assay; Cytometry was used to detect cell apoptosis. Bioinformatics methods were used to explore the possible signaling pathways involved in the regulation of AIPC proliferation by TCP1-β. Results: (1) After the removal of androgen, the proliferation of LnCap cells was significantly inhibited, while the proliferation of PC3 cells was not significantly affected. ② After transfected with TCP1-β siRNA, the expression of TCP1-β was significantly inhibited in PC3-Ad and LnCap cells = 0.002, P = 0.006); ③PC3-Ad significantly inhibited the expression of TCP1-β, the cell proliferation was inhibited (P = 0.015), but the cells did not show significant apoptosis; TCP1-β expression inhibited the proliferation of LnCap cells And apoptosis had no significant effect; ④TCP1-β may be involved in the regulation of PI3K / Akt signaling pathway on the proliferation of AIPC. Conclusion: Overexpression of TCP1-β may be involved in the regulation of proliferation of AIPC cells.