Journal
EXPERIMENTAL AND THERAPEUTIC MEDICINE
Volume 14, Issue 3, Pages 2702-2708Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2017.4828
Keywords
breast cancer; microRNA; estrogen receptor alpha; viability; migration; invasion
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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 a (ER alpha)-positive breast cancer cells were investigated. It was found that treatment with estradiol (E2) significantly enhanced the viability, migration and invasion of ER alpha-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 ERa in MCF-7 cells. Using a luciferase reporter assay, ER alpha was identified as a direct target of miR-203 in MCF-7 cells. Finally, it was demonstrated that miR-203 was significantly down regulated in ER alpha-positive breast cancer tissues compared to their matched normal adjacent tissues. The expression levels of miR-203 were inversely correlated to the ER alpha levels in ER alpha-positive breast cancer tissues. Based on these results, it is proposed that miR-203 inhibits E2-induced viability, migration and invasion of ER alpha-positive breast cancer cells, and that this may be via direct targeting of ER alpha. Therefore, the present study highlights the importance of miR-203 and ER alpha in breast cancer progression.
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