祝贺勇山公司于《Cell Signaling》成功发表科研论文

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

Gaoyong Liao, Mengyu Wang, Yu Ou, Yong Zhao.

Cell Signaling 26 (2014) 2131-2137

Abstract

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 upregulatesMUC1 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 β-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.

Copyright © 2014. Published by Elsevier Inc.

KEYWORDS:

EMT; ERK; IGF-1; MUC1; Migration; PI3K/Akt