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

Authors: Wang, Yingmei  Zhu, Yuanxi  Zhang, Lizhi  Tian, Wenyan  Hua, Shaofang  Zhao, Jing  Zhang, Huiying  Xue, Fengxia 
Citation: Wang Y, etal., Cancer Lett. 2012 Sep 28;322(2):223-31. doi: 10.1016/j.canlet.2012.03.026. Epub 2012 Mar 27.
Pubmed: (View Article at PubMed) PMID:22459351
DOI: Full-text: DOI:10.1016/j.canlet.2012.03.026

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·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·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.


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RGD Object Information
RGD ID: 13441552
Created: 2017-10-26
Species: All species
Last Modified: 2017-10-26
Status: ACTIVE


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