Format

Send to

Choose Destination
Exp Ther Med. 2017 Sep;14(3):2702-2708. doi: 10.3892/etm.2017.4828. Epub 2017 Jul 24.

MiR-203 inhibits estrogen-induced viability, migration and invasion of estrogen receptor α-positive breast cancer cells.

Author information

1
Department of Breast Surgery, Yantai Yuhuangding Hospital, Yantai, Shandong 264001, P.R. China.
2
Department of Hematology, Yantai Yuhuangding Hospital, Yantai, Shandong 264001, P.R. China.

Abstract

Breast cancer is common in females, and accounts for a large proportion of cancer-related cases of mortality. MicroRNAs (miRs) have been found to be involved in the progression of breast cancer via mediation of tumor suppressor genes or oncogenes. Previously, miR-203 has been reported to play a suppressive role in breast cancer. In the present study, the effects of miR-203 on the malignant phenotypes of estrogen receptor α (ERα)-positive breast cancer cells were investigated. It was found that treatment with estradiol (E2) significantly enhanced the viability, migration and invasion of ERα-positive breast cancer MCF-7 cells, accompanied by the significant downregulation of miR-203 in a dose-dependent manner. Furthermore, MCF-7 cells were transfected with miR-203 mimics, resulting in a significant increase in miR-203 levels. Upregulation of miR-203 was found to significantly inhibit E2-induced upregulation of MCF-7 cell viability, migration and invasion. Upregulation of miR-203 also led to a significant decrease in the protein expression of ERα in MCF-7 cells. Using a luciferase reporter assay, ERα was identified as a direct target of miR-203 in MCF-7 cells. Finally, it was demonstrated that miR-203 was significantly downregulated in ERα-positive breast cancer tissues compared to their matched normal adjacent tissues. The expression levels of miR-203 were inversely correlated to the ERα levels in ERα-positive breast cancer tissues. Based on these results, it is proposed that miR-203 inhibits E2-induced viability, migration and invasion of ERα-positive breast cancer cells, and that this may be via direct targeting of ERα. Therefore, the present study highlights the importance of miR-203 and ERα in breast cancer progression.

KEYWORDS:

breast cancer; estrogen receptor α; invasion; microRNA; migration; viability

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center