摘要
目的 :探讨乳腺癌细胞中ERK/MAPK信号转导通路异常激活与乳腺癌细胞浸润性生长的关系及可能机制。 方法 :采用Western蛋白印迹技术检测乳腺癌细胞系MCF 7和MDA MB 4 35S中磷酸化ERK/MAPK(p ERK)蛋白表达 ,以及表皮生长因子 (EGF)、胰岛素样生长因子 1(IGF 1)和ERK/MAPK通路抑制剂PD980 5 9对两种细胞ERK/MAPK信号转导通路磷酸化的调节。 结果 :雌激素受体ER(- )的浸润性乳腺癌细胞系MDA MB 4 35S中 ,p ERK表达明显高于ER(+)的非浸润性乳腺癌细胞系MCF 7;EGF可刺激两种细胞p ERK的表达增加 ,但这种刺激作用在MDA MB 4 35S细胞中更加明显 ;IGF 1则仅能刺激MCF 7细胞中p ERK的表达。PD980 5 9能有效阻滞EGF、IGF 1对p ERK的激活。 结论 :ERK/MAPK信号转导通路的异常激活与乳腺癌的浸润性生长有关 ,而EGF可能是异常激活ERK/MAPK信号转导通路 ,是刺激ER(- )的乳腺癌细胞浸润性生长的重要因素之一。
Objective:To address the relationship between ERK/MAPK phosphorylation (p-ERK) and the invasive growth of human breast cancer cells and its possible mechanism. Methods:The protein expressions of p-ERK in human breast cancer cell MCF-7 and MDA-MB- 435s were examined and the regulations of EGF, IGF-1 and ERK/MAP kinase specific inhibitor , PD98059 on these two kinds of cells. Results:Compared with ER-positive and no-invasive MCF-7 cells, the ER-negative and invasive MDA-MB- 435s cells had higher p-ERK protein expression. EGF stimulation induced more p-ERK activation in MDA-MB- 435s cells than that in MCF-7 cells. But IGF-1 only actived p-ERK signal transduction pathway in MCF-7 cells obviously. Treatment with PD98059 could block this activation in the two kinds of cells. Conclusion :The increasing of p-ERK activity was related to the malignant invasive growth of breast cancer cells and EGF was one of the important factors to activate ERK/MAPK signal transduction pathway to promote the cell invasive proliferation.
出处
《医学研究生学报》
CAS
2004年第6期490-492,共3页
Journal of Medical Postgraduates
关键词
乳腺癌
丝裂素活化蛋白激酶
信号转导
浸润性生长
Breast cancer
Mitogen-activated protein kinase
Signal transduction
Invasive growth
