阻断MAPK通路对前列腺癌细胞增殖的影响

目的：研究前列腺癌进展中细胞丝裂原活化蛋白激酶(MAPK)信号通路的变化，探讨阻断此通路对前列腺癌细胞增殖的影响。方法：用MTT法检测表皮生长因子（EGF）、PD98059对前列腺癌细胞系LNCaP、PC 3和DU145增殖的影响；用Western blot法检测细胞外信号调节激酶1/2（ERK1/2）表达和磷酸化ERK1/2水平的差异，以及EGF、PD98059对细胞ERK1/2磷酸化水平的影响。结果：EGF促进LNCaP、PC 3和 DU145的增殖，PD98059抑制细胞增殖；Western blot结果显示，3株前列腺癌细胞的总ERK1/2无明显差异。在血清饥饿的状态下，LNCaP细胞无ERK1/2的活化,而PC 3和 DU145细胞ERK1/2处于持续活化的状态。PD98059能够阻断EGF对3株前列腺癌细胞ERK1/2的激活。结论：MAPK通路的持续活化在前列腺癌的恶性进展中起重要作用，阻断此通路可以抑制前列腺癌细胞的增殖。

Blocking of the mitogen activated protein kinase signal transduction pathway inhibits the proliferation in the prostate cancer cells

Objective: To investigate the change of mitogen activated protein kinase(MAPK) signaling pathway during prostate cancer progression,and therefore to explore its role on cell proliferation.Methods: MTT assay was used to examine the effects of epidermal growth factor(EGF) and PD98059 on proliferation of prostate cancer cell lines LNCaP,PC-3 and DU145,and western blotting to detect the level of total extracellular signal-regulated kinase 1/2(ERK1/2),the level of phospho-ERK1/2 before and after the EGF stimulation and PD98059 inhibition.Results: EGF promoted the prostate cancer cell growth,whereas PD98059 inhibited the cell growth and stopped the EGF from stimulating the LNCaP,PC-3 and DU145 cells. The total ERK1/2 level was not significantly different in the three cell lines,whereas the phospho-ERK1/2 was not detected with western blotting in LNCaP cell line and ERK1/2 activity was found in PC-3 and DU145.Conclusion: The MAPK transpass activity is promoted during the prostate cancer progression,suggesting that blocking the MAPK transpass can be used as a method for prostate cancer therapy.