MiR-519 regulates the proliferation of breast cancer cells via targeting human antigen R.

Abstract

Breast cancer is one of the most prevalent types of cancer among women that leads to millions of deaths worldwide every year. The mechanisms of breast cancer pathogenesis remain unclear. It has been reported that aberrant expression of miR-519, is associated with breast cancer development; however, the effects of miR-519 on breast cancer cell proliferation remain unknown. Therefore, the present study aimed to determine whether miR-519 could regulate breast cancer cell proliferation. A total of 20 pairs of primary breast cancer and adjacent normal tissues were collected from patients with breast cancer. miR-519 expression level was determined by reverse transcription-quantitative polymerase chain reaction. Furthermore, miR-519 mimics or inhibitors were transfected into breast cancer MCF-7 cells in order to up- or downregulate miR-519 expression. Subsequently, human antigen R (HUR), BCL-2 and BAX protein levels were analyzed by western blotting. MCF-7 cell proliferation was assessed using MTT and colony formation assays. A luciferase assay was performed to verify whether miR-519 could directly bind to HUR mRNA. The results demonstrated that miR-519 expression level was lower in primary breast cancer tissues compared with adjacent normal tissues. Furthermore, miR-519 overexpression and downregulation inhibited and stimulated MCF-7 cell proliferation, respectively. In addition, the results from luciferase assay demonstrated that HUR was a target of miR-519. HUR overexpression could reverse the effect of miR-519 mimics on MCF-7 cell proliferation, whereas HUR silencing could rescue the effect of miR-519 inhibitors on MCF-7 cell proliferation. These findings suggested that miR-519 may regulate MCF-7 cell proliferation by targeting HUR.