Document Detail

The expression and role of hybrid insulin/insulin-like growth factor receptor type 1 in endometrial carcinoma cells.
MedLine Citation:
PMID:  20620597     Owner:  NLM     Status:  MEDLINE    
Insulin receptor (IR) and type 1 insulin-like growth factor receptor (IGF-IR) can assemble heteromerically as a hybrid insulin/IGF-I receptor (hybrid-R) in tissues that express both molecules. There is little information about hybrid-R in endometrial carcinoma, in which both IR and IGF-IR are frequently overexpressed. We used immunoprecipitation to detect hybrid-R expression in two endometrial carcinoma cell lines: HEC-1a, which has low estrogen receptor (ER) expression, and Ishikawa, which is positive for ER expression. To explore the role of hybrid-R in endometrial carcinoma cells, we examined phosphorylation of extracellular signal-regulated kinase (ERK1/2), which is a key molecule in the mitogen-activated protein kinase (MAPK) pathway. The effect of inhibiting IGF-I, IGF-II, and insulin on cell cycle progression and apoptosis was assessed by flow cytometry. Both cell lines expressed hybrid-R, and HEC-1a cells had higher expression levels than did Ishikawa cells. IGF-I induced ERK1/2 phosphorylation in HEC-1a cells mainly through hybrid-R; in Ishikawa cells, this effect was mediated only in part by hybrid-R. Insulin stimulated ERK1/2 phosphorylation partly through hybrid-R in HEC-1a cells, but not in Ishikawa cells. Both IGFs and insulin increased cellular DNA content in the S phase of the cell cycle in HEC-1a through hybrid-R. In contrast, in Ishikawa cells, only insulin enhanced DNA content in S phase through hybrid-R. Both IGFs and insulin significantly decreased apoptosis in HEC-1a cells through hybrid-R, and a similar but moderate effect was observed in Ishikawa cells. Hybrid-R, which is present in endometrial carcinoma cells, may have an important role in mediating IGF- and insulin-induced cell growth and in preventing apoptosis.
Guo Zhang; Xiaoping Li; Lili Zhang; Lijun Zhao; Jing Jiang; Jianliu Wang; Lihui Wei
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cancer genetics and cytogenetics     Volume:  200     ISSN:  1873-4456     ISO Abbreviation:  Cancer Genet. Cytogenet.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-12     Completed Date:  2010-07-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7909240     Medline TA:  Cancer Genet Cytogenet     Country:  United States    
Other Details:
Languages:  eng     Pagination:  140-8     Citation Subset:  IM    
Copyright Information:
Copyright (c) 2010 Elsevier Inc. All rights reserved.
Department of Gynecology, Peking University People's Hospital, No. 11 Xi-Zhi-Men South Street, Xi Cheng District, Beijing, China.
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MeSH Terms
Apoptosis / drug effects
Cell Cycle / drug effects
Cell Line, Tumor
Endometrial Neoplasms / pathology*
Extracellular Signal-Regulated MAP Kinases / metabolism
Insulin / pharmacology
Insulin-Like Growth Factor I / pharmacology
Receptor, IGF Type 1 / analysis,  genetics*,  physiology
Receptor, Insulin / analysis,  genetics*,  physiology
Recombinant Fusion Proteins / physiology*
Reg. No./Substance:
0/Recombinant Fusion Proteins; 11061-68-0/Insulin; 67763-96-6/Insulin-Like Growth Factor I; EC, IGF Type 1; EC, Insulin; EC Signal-Regulated MAP Kinases

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