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MicroRNA-206 inhibits metastasis of triple-negative breast cancer by targeting transmembrane 4 L6 family member 1

Authors Fan C, Liu N, Zheng D, Du J, Wang K

Received 20 December 2018

Accepted for publication 4 May 2019

Published 22 July 2019 Volume 2019:11 Pages 6755—6764

DOI https://doi.org/10.2147/CMAR.S199027

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Cristina Weinberg

Peer reviewer comments 2

Editor who approved publication: Dr Teng


Chunni Fan,1 Ning Liu,1 Dan Zheng,1 Jianshi Du,2 Keren Wang1

1Department of Breast Surgery, China‑Japan Union Hospital of Jilin University, Changchun, Jilin Province 130033, People’s Republic of China; 2Department of Vascular Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province 130033, People’s Republic of China

Purpose: Breast cancer (BC) is a common malignancy in women, but the survival rate for BC is not very encouraging. Especially for triple-negative breast cancer (TNBC), a kind of breast cancer that does not have any of the receptors that are commonly found in BC. We investigated the impact of microRNA-206 (miR-206) on transmembrane 4 L6 family member 1 (TM4SF1) in TNBC for therapeutic purpose.
Patients and methods: Twenty BC tissues from diagnosed BC patients were analyzed via real-time PCR and Western blotting for expression of TM4SF1 and miR-206. The expression of TM4SF1 was studied in relationship with miR-206 in MDA-MB-231 cells. The biological impact of TM4SF1 and miR-206 on MDA-MB-231 cells and BALB/c nude mice model was studied using proliferation, transwell migration, and invasion assays both in vitro and in vivo.
Results: The expression of TM4SF1 in BC tissues was significantly higher than that in adjacent normal breast tissues. In contrast, miR-206 showed a decreased expression level in BC tissues, especially for subtype basal like. Overexpression of miR-206 in MDA-MB-231 cells by transfecting miR-206 resulted in downregulation of TM4SF1. In contrast, knockdown miR-206 expression reversed miR-206-mediated phenotype in MDA-MB-231 cells. Expression level of TM4SF1 in MDA-MB-231 cells was associated with cell migration and invasion capabilities in vitro. Breast tumor burden was correlated with the expression level of TM4SF1 in vivo.
Conclusion: Taken together, our results showed the involvement of TM4SF1 in TNBC migration and invasion. miR-206 negatively regulated gene expression of TM4SF1. These findings indicate that miR-206 could be used as a potential therapeutic agent for TNBC.

Keywords: miR-206, TM4SF1, TNBC, migration, invasion


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