Insulin promotes proliferation, survival, and invasion in endometrial carcinoma by activating the MEK/ERK pathway

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• 作者：Yingmei Wang^a ; ¹ ; Yuanxi Zhu^b ; ¹ ; Lizhi Zhang^c ; Wenyan Tian^a ; Shaofang Hua^d ; Jing Zhao^a ; Huiying Zhang^a ; Fengxia Xue^a ; ^{fengxiaxue1962@163.com}
• 关键词：Endometrial carcinoma ; Insulin ; MEK/ERK pathway ; Proliferation ; Invasion
• 出版年：2012
• 期刊代码：44_03043835
• 类别：med
• 出版时间：28 September, 2012
• 卷：322
• 期：2
• 页码：223-231
• 文件大小：928 K

摘要

The involvement of insulin in endometrial carcinoma (EC) was investigated using radioimmunoassay, Western blot, immunoprecipitation, MTT, and Annexin V-FITC/PI assays in tissue samples and cultured cells. Serum levels of insulin, p-p52Shc, p-p46Shc, Shc路Grb2 complexes, p-MEK, p-ERK, and cyclin D1 were elevated in patients with EC. Expression of key proteins in the MEK/ERK pathway, including p-p52Shc, Shc路Grb2 complexes, p-MEK, p-ERK, and cyclin D1, was significantly higher in patients with advanced FIGO stage, high grade, and lymph-node metastasis and correlated positively with serum insulin concentration. Insulin promotes Ishikawa 3-H-12 cell proliferation, survival, and invasion, and these effects induced by insulin were significantly blocked by MEK inhibitor PD98059. Insulin thus promotes EC cell proliferation, survival, and invasion via the MEK/ERK pathway.