GATA1 induces epithelial-mesenchymal transition in breast cancer cells through PAK5 oncogenic signaling

作者：Yang Li, Yang Li, Qiang Ke, Yangguang Shao, Ge Zhu, Yanshu Li, Yanshu Li, Nanxi Geng, Feng Jin, Feng Li · 发表于：Oncotarget · 年份：2015 · DOI：10.18632/oncotarget.2999 · 被引用次数：59 · 研究领域：Metastasis and carcinoma case studies、Cancer Cells and Metastasis、Mechanisms of cancer metastasis

// Yang Li 1, * , Qiang Ke 1, * , Yangguang Shao 1 , Ge Zhu 1 , Yanshu Li 1 , Nanxi Geng 1 , Feng Jin 2 , Feng Li 1 1 Department of Cell Biology, Key Laboratory of Cell Biology, Ministry of Public Health and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China 2 Department of Breast Surgery, Department of Surgical Oncology, Research Unit of General Surgery, The First Affiliated Hospital of China Medical University, Shenyang, China * These authors have contributed equally to this work Correspondence to: Feng Li, e-mail: fli@mail.cmu.edu.cn Keywords: EMT, Breast cancer, GATA1, PAK5, Phosphorylation Received: October 01, 2014      Accepted: December 21, 2014      Published: January 21, 2015 ABSTRACT Epithelial-mesenchymal transition (EMT) is a key process in tumor metastatic cascade that is characterized by the loss of cell-cell junctions, resulting in the acquisition of migratory and invasive properties. E-cadherin is a major component of intercellular junctions and the reduction or loss of its expression is a hallmark of EMT. Transcription factor GATA1 has a critical anti-apoptotic role in breast cancer, but its function for metastasis has not been investigated. Here, we found that GATA1, as a novel E-cadherin repressor, promotes EMT in breast cancer cells. GATA1 binds to E-cadherin promoter, down-regulates E-cadherin expression, disrupts intercellular junction and promotes me...