Oncotarget

Research Papers:

MiR-206 suppresses epithelial mesenchymal transition by targeting TGF-β signaling in estrogen receptor positive breast cancer cells

Kai Yin _, Wenjin Yin, Yaohui Wang, Liheng Zhou, Yu Liu, Gong Yang, Jianhua Wang and Jinsong Lu

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Oncotarget. 2016; 7:24537-24548. https://doi.org/10.18632/oncotarget.8233

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Abstract

Kai Yin1,2, Wenjin Yin1,2, Yaohui Wang3, Liheng Zhou3, Yu Liu3, Gong Yang4,5, Jianhua Wang4, Jinsong Lu3

1Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China

2Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China

3Breast Cancer Center, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China

4Cancer Institute, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China

5Central Laboratory, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China

Correspondence to:

Jinsong Lu, e-mail: lujjss@163.com

Jianhua Wang, e-mail: jianhuawang2007@qq.com

Gong Yang, e-mail: yanggong@fudan.edu.cn

Keywords: breast cancer, miRNA, epithelial mesenchymal transition, TGF-β, migration

Received: September 14, 2015     Accepted: March 04, 2016     Published: March 21, 2016

ABSTRACT

Background: Previous reports have shown a mutual negative feedback loop between microRNA (miR)-206 and estrogen receptor (ER) expression. Furthermore, decreased miR-206 expression in breast cancer (BC) is associated with the advanced clinical stage and lymph node metastasis. However, its role and the mechanism underlying the migration and invasion of ER positive BC remain unclear.

Results: In this study, miR-206 was stably transfected into ER positive cell lines MCF-7 and T47D to investigate the effect of miR-206. The results showed that miR-206 overexpression markedly impaired the migration and invasive abilities of these cells, followed by suppression of the epithelial mesenchymal transition (EMT). Mechanistic analyses showed that miR-206 inhibited the autocrine production of transforming growth factor (TGF)-β as well as the downstream expression of neuropilin-1 (NRP1) and SMAD2, responsible for the decreased migration, invasion, and EMT in these cells.

Conclusions: Our data demonstrate that miR-206 inhibits TGF-β transcription and autocrine production, as well as downstream target genes of EMT. Restoring miR-206 expression may provide an effective therapeutic strategy for ER positive BC.


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