MAPK/ERK通路
MCF-7型
激酶
胰岛素
胰岛素受体
信号转导
磷酸化
细胞生长
丝裂原活化蛋白激酶
癌症研究
化学
内科学
细胞生物学
生物
内分泌学
癌细胞
医学
胰岛素抵抗
癌症
生物化学
人体乳房
作者
Hui Chen,Zhenwen Zhang,Yuan Guo,Yan Wang,Yan Liu,Na Luo,Yun Zhu
出处
期刊:PubMed
日期:2013-01-22
卷期号:17 (4): 658-62
被引量:3
摘要
To explore the proliferative role of insulin and the potential mechanism in human breast cancer cell line MCF-7.MCF-7 cells were treated with different concentrations of insulin. Morphological observation and methylthiazolyltetrazolium (MTT) assay were used to detect the proliferation of MCF-7 cells. The expression of insulin receptor mRNA was detected by RT-PCR, with or without mitogen activated kinase (MAPK) signals blocked by their inhibitors: SP600125, the inhibitor of Jun N-terminal kinase (JNK), and PD98059, the inhibitor of extracellular signal-regulated (ERK1/2).Insulin increased the proliferation of MCF-7 cells in a concentration-independent manner. Western blotting implicated that 100 nM insulin induced activation of JNK and ERK. The expression of phosphorylated JNK was detected within 5 min after insulin treatment and sustained for an hour, while ERK was activated later than JNK, at the 30th min after insulin treatment. Then we reevaluated the proliferative effect promoted by insulin after MAPK signaling pathway was blocked by its inhibitors. The results showed that after inhibiting the activities of JNK and ERK, the proliferative effect of insulin was also attenuated. Western blot results showed that, while blocking the MAPK signaling pathway, 10 μM (ERK pathway inhibitor) could significantly inhibit phosphorylated activation of ERK1/2 with 200 nM insulin at 30 min, while no obvious inhibition with 20 μM SP600125 (JNK pathway inhibitor) of phosphorylated activation of ERK1/2 was noticed.It seems that insulin can stimulate the proliferation of MCF-7 cells in vitro. MAPK signal transduction pathway involves the proliferative effect, which also regulates the expression of insulin receptor, mediates and amplifies the insulin signaling pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI