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山东大学学报(医学版)

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阻断MAPK通路对前列腺癌细胞增殖的影响

高庆贞1, 吕家驹2, 张辉2, 尉立京2,丁克家2   

  1. 山东大学 1. 临床医学院济南市中心医院血液净化中心,山东 济南 250013;2. 山东省立医院泌尿外科,山东 济南 250021
  • 收稿日期:2005-09-14 修回日期:1900-01-01 出版日期:2006-05-24 发布日期:2006-05-24
  • 通讯作者: 高庆贞

GAO Qing-zhen,Jia-ju2, ZHANGHui2, WEI Li-jing2, DING Ke-jia2   

  1. 1. Blood Purification Center, Jinan Central Hospital, Shandong University, Jinan 250013, Shandong, China;2.Department of Urology, Shandong Provincial Hospital, Shandong University, Jinan 250021, Shandong, China
  • Received:2005-09-14 Revised:1900-01-01 Online:2006-05-24 Published:2006-05-24
  • Contact: GAO Qing-zhen

摘要: 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。

Abstract: 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.

Key words: Prostatic neoplasms, Protein kinases, Mitogens

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