Open AccessMiR-205 suppressed the malignant behaviors of breast cancer cells by targeting CLDN11 via modulation of the epithelial-to-mesenchymal transition
Author(s) -
Yimin Shen,
Yingchun Xu,
Liming Huang,
Yongxin Chi,
Meng Li
Publication year - 2021
Publication title -
aging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.473
H-Index - 90
ISSN - 1945-4589
DOI - 10.18632/aging.202988
Subject(s) - epithelial–mesenchymal transition , cancer research , mesenchymal stem cell , modulation (music) , breast cancer , transition (genetics) , chemistry , microbiology and biotechnology , cancer , biology , medicine , physics , metastasis , gene , biochemistry , acoustics
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.