GM-CSF引起的MAPK途径磷酸化在激素非依赖性前列腺癌增殖中的作用

Role of MAPK Signal Transduction Pathway Phosphorylation Induced by Granulocyte-macrophage-colony Stimulating Factor in the Proliferation of Hormone-Independent Prostate Cancer

目的:研究丝裂原活化蛋白激酶(MAPK)信号途径中Erk1/2分子磷酸化在粒细胞-单核细胞集落刺激因子(GM-CSF)促进前列腺癌增殖中的作用。方法:前列腺癌PC-3M细胞经过GM-CSF刺激前后,流式细胞术和半定量RT-PCR分别检测细胞周期和细胞周期蛋白K i-67表达的变化;W estern印迹法对比GM-CSF作用前后Erk1/2分子磷酸化程度的变化。结果:GM-CSF可以显著增加PC-3M细胞S期和G2/M期的百分率以及K i-67蛋白的表达,同时Erk1/2分子磷酸化程度显著增强。结论:Erk1/2分子磷酸化可能是GM-CSF促进前列腺癌增殖的重要分子机制。

Objective： To investigate the phosphorylation intensity of MAPK pathway molecular Erk1/2 and the proliferation of prostate cancer cell line PC-3M. Methods ： Flowcytometry and RT-PCR were employed to study the ratio of different cell cycles and phases, respectively, before and after GM-CSF stimulation. Erk1/2 phosphorylation intensity was examined by Western blot simultaneously. Results： The rate of PC-3M cells at S and G2/M stages and the expression intensity of Ki-67 increased after GM-CSF incubation in a dose-dependent manner. The phosphorylation intensity of Erkl/2 increased remarkably after stimulation with GM-CSF. Conclusion ： The intensification of Erkl/2 phosphorylation is one important molecular mechanism of the proliferation of hormone-independent prostate cancer.