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Research Paper|Volume 13, Issue 9|pp 13073—13086

MiR-205 suppressed the malignant behaviors of breast cancer cells by targeting CLDN11 via modulation of the epithelial-to-mesenchymal transition

Yupeng Shen1, Yingchun Xu2, Liming Huang2, Yongxin Chi2, Liwei Meng2
  • 1Medical School of Shaoxing University, Yuecheng, Shaoxing 312000, Zhejiang Province, People’s Republic of China
  • 2Department of Breast and Thyroid Surgery, Shaoxing People's Hospital, The First Affiliated Hospital of Shaoxing University, Shaoxing 312000, Zhejiang Province, People’s Republic of China
* Equal contribution
Received: November 20, 2020Accepted: March 27, 2021Published: May 8, 2021
https://doi.org/10.18632/aging.202988

Copyright: © 2021 Shen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Some Aberrant expression of miRNAs plays an important role in the occurrence and distant metastasis of breast cancer. This study aimed to identify crucial miRNA signatures for breast cancer using microarray data from the Gene Expression Omnibus database, including ductal carcinoma in situ and invasive duct carcinoma. In this study, we founded that miR-205 was significantly down-regulated in breast cancer, and the low expression of miR-205 was significantly associated with the TNM stage of breast cancer. In vitro, functional studies revealed that over-expression of miR-205 inhibited the proliferation and promoted apoptosis of breast cancer cells MDA-MB-231. Mechanistically, claudin 11 (CLDN11) was found to be the direct target of miR-205; the function of miR-205 could be exerted via downregulation of the target gene CLDN11 in breast cancer cells. Furthermore, the over-expression of miR-205 promoted the expression of the epithelial marker E-cadherin but reduced the mesenchymal markers in breast cancer cells. These results collectively indicated the tumor-suppressive role of miR-205 in breast cancer by targeting CLDN11; implying miR-205 may serve as a novel therapeutic target for breast cancer.