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

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.