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目的:探讨微小RNA(mi R)-204对前列腺癌细胞株CL1的生长调节及其机理。方法:获得mi R-204高表达的CL1稳转细胞株(CL1-mi R-204)及其阴性对照的CL1稳转细胞株(CL1-对照)后,观察其细胞生长速度,检测丝氨酸/苏氨酸蛋白激酶(AKT)磷酸化水平及AKT总蛋白和p27蛋白的表达,并检测磷脂酰肌醇3-激酶(PI3K)通道抑制剂LY294002对2种细胞生长的影响。结果:mi R-204能促进CL1的生长;升高AKT在苏氨酸(T308)和丝氨酸(S473)2个位点的磷酸化水平;抑制AKT下游的靶基因p27蛋白表达水平。加入LY294002后,CL1-对照和CL1-mi R-204的生长速度都降低。但CL1-mi R-204的生长速度下降得更明显。结论:mi R-204可能是通过AKT信号通路来促进CL1的生长。
Objective: To investigate the regulation of microRNA (mi R) -204 on the growth of prostate cancer cell line CL1 and its mechanism. Methods: The CL1-mi R-204 cell line (CL1-mi R-204) and its negative control CL1 stable cell line (CL1-control) were obtained and the cell growth rate was observed. Phosphorylation of AKT and the expression of AKT total protein and p27 protein, and the effect of PI3K channel inhibitor LY294002 on the growth of the two kinds of cells. Results: mi R-204 promoted the growth of CL1, increased the phosphorylation of AKT at the two sites of threonine (T308) and serine (S473), and inhibited the expression of p27 protein downstream of AKT. After adding LY294002, the growth rates of CL1-control and CL1-mi R-204 all decreased. However, the growth rate of CL1-mi R-204 decreased more significantly. Conclusion: mi R-204 may promote the growth of CL1 through the AKT signaling pathway.