IGF-1-induced epithelial-mesenchymal transition in MCF-7 cells is mediated by MUC1

被引:35
|
作者
Liao, Gaoyong [1 ,2 ,3 ,4 ]
Wang, Mengyu [2 ,3 ,4 ]
Ou, Yu [1 ]
Zhao, Yong [2 ,3 ,4 ]
机构
[1] China Pharmaceut Univ, Sch Life Sci & Technol, Nanjing 210009, Jiangsu, Peoples R China
[2] Simcere Pharmaceut Co Ltd, Nanjing, Jiangsu, Peoples R China
[3] BioSciKin Co Ltd, Nanjing, Jiangsu, Peoples R China
[4] MtC BioPharma Co Ltd, Nanjing, Jiangsu, Peoples R China
关键词
IGF-1; MUC1; EMT; Migration; PI3K/Akt; ERK; CARCINOMA-ASSOCIATED ANTIGEN; BREAST-CANCER CELLS; FACTOR-I RECEPTOR; BETA-CATENIN; GROWTH; EXPRESSION; ADHESION; INVASION; OVEREXPRESSION; ONCOPROTEIN;
D O I
10.1016/j.cellsig.2014.06.004
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Metastases are the major cause of death from cancer. IGF-1 signaling pathway has been shown to have strong implication in the epithelial-mesenchymal transition (EMT) process. However, the mechanisms of how IGF-1 promotes EMT have not been fully elucidated. Mucin 1 (MUC1), a transmembrane glycoprotein, engages in multiple cancer-related signaling pathways and functions as an oncoprotein that contributes to metastases. Here we provide evidence showing that IGF-1 upregulates MUC1 expression in MCF-7 cells in a PI3K/Akt signaling pathway-dependent manner. The overexpression of MUC1 is critical for IGF-1-induced EMT of MCF-7 cells because the knockdown of MUC1 prevented the EMT of MCF-7 cells as demonstrated by various EMT markers including the expression of E-cadherin, N-cadherin, vimentin, fibronectin and the nuclear translocalization of beta-catenin. On the other hand, the knockdown of MUC1 had no impact on IGF-1-induced activation of PI3K/Akt or MAPK. In summary, our study demonstrated MUC1 as a critical downstream effector that mediates IGF-1-induced EMT of MCF-7 cells and suggested that MUC1 might be a potential therapeutic target for preventing tumor metastases. (C) 2014 Elsevier Inc All rights reserved.
引用
收藏
页码:2131 / 2137
页数:7
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