IR@PKUHSC  > 北京大学第二临床医学院
学科主题临床医学
Overexpression of the Insulin Receptor Isoform A Promotes Endometrial Carcinoma Cell Growth
Wang, Chun-Fang; Zhang, Guo; Zhao, Li-Jun; Qi, Wen-Juan; Li, Xiao-Ping; Wang, Jian-Liu; Wei, Li-Hui
刊名PLOS ONE
2013-08-07
DOI10.1371/journal.pone.0069001
8期:8
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]IGF-II ; CANCER ; PATHWAY ; EXPRESSION ; INHIBITORS ; APOPTOSIS
英文摘要

Epidemiological studies have demonstrated that type 2 diabetes mellitus (T2DM) and hyperinsulinemia are associated closely with endometrial carcinoma risk, although the molecular mechanism remains unclear. Insulin receptor isoformA expression is upregulated in many cancer cells and tissues, which suggests that IR-A-mediated signaling pathways may have important implications for cancer pathogenesis. We measured the expression of insulin receptor isoforms (IR-A and IR-B in the normal endometrium tissues, the endometrial carcinoma tissues and the endometrial carcinoma cell lines. We found that the total insulin receptor (IR) and IR-A expression mRNA levels and the ratio of IR-A to total IR in endometrial carcinoma specimens were significantly higher than them in control endometrial tissue specimens(P<0.05). Further analysis indicated that the tendency was more prominently in patients with T2DM. IR-A mRNA was differentially expressed in four endometrial carcinoma cell lines (Ishikawa, KLE, RL95-2 and HEC-1-A. RL95-2 cells have a low endogenous IR-A expression, and these were used to construct a stable cell line overexpressing IR-A. We found that IR-A overexpression significantly increased cell proliferation, the proportion of cells in S phase, activation of the Akt pathway and tumorigenicity of xenografts in nude mice. In contrast, there was no significant difference in the the percentage of apoptotic cells between cells overexpressing IR-A and control cells. Moreover, levels of phosphorylated ERK1/2 protein were significantly decreased in cells overexpressing IR-A relative to controls. These findings reveal the pivotal role of IR-A in endometrial cancer carcinogenesis, and suggest that the association of elevated IR-A levels with cell proliferation and tumorigenicity may be causally linked to its effect on the proportion of cells in S phase and the activation of the Akt pathway.

语种英语
WOS记录号WOS:000323109700012
Citation statistics
Cited Times:5[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/57706
Collection北京大学第二临床医学院
作者单位Peking Univ, Dept Obstet & Gynecol, Peking Univ Peoples Hosp, Beijing 100871, Peoples R China
Recommended Citation
GB/T 7714
Wang, Chun-Fang,Zhang, Guo,Zhao, Li-Jun,et al. Overexpression of the Insulin Receptor Isoform A Promotes Endometrial Carcinoma Cell Growth[J]. PLOS ONE,2013,8(8).
APA Wang, Chun-Fang.,Zhang, Guo.,Zhao, Li-Jun.,Qi, Wen-Juan.,Li, Xiao-Ping.,...&Wei, Li-Hui.(2013).Overexpression of the Insulin Receptor Isoform A Promotes Endometrial Carcinoma Cell Growth.PLOS ONE,8(8).
MLA Wang, Chun-Fang,et al."Overexpression of the Insulin Receptor Isoform A Promotes Endometrial Carcinoma Cell Growth".PLOS ONE 8.8(2013).
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