miR-4709-3p Inhibits Cell Proliferation by Downregulating Expression in Breast Cancer Cells.

Breast cancer is a serious threat to the physical and mental health of women all over the world. Our previous results have shown that Serine protease 50 (), an oncogene overexpressed in breast cancer, can promote proliferation, migration, and invasion of breast cancer cells. Mechanistic studies have revealed that promoted tumorigenesis mainly by activating NF-kappa B (NF-κB) and inhibiting activin signaling pathway, indicating that played a critical role in the occurrence and development of breast cancer. However, there are few reports on the regulation of expression in breast cancer. MicroRNAs (miRNAs) have emerged as an essential posttranscriptional regulator in gene expression and they played a significant role in breast cancer regulation. In the present study, bioinformatics software miRBase and TargetScan were first used to predict and analyze miRNAs that could target mRNA 3'UTR and six miRNAs were found. Results from quantitative real-time PCR (qRT-PCR) and western blot suggested that miR-4709-3p could bind to mRNA 3'UTR and significantly inhibit the expression of protein. Moreover, the effects of miR-4709-3p on the proliferation of breast cancer cells and mammary epithelial cells were detected . Our data suggested that overexpression of miR-4709-3p mimic greatly inhibited the proliferation of breast cancer cells, whereas overexpression of miR-4709-3p inhibitors significantly promoted the proliferation of breast epithelial cells. Furthermore, the effect of miR-4709-3p on the tumorigenicity of breast cancer cells was tested, and the results showed that miR-4709-3p significantly reduced the volume and weight of tumor in nude mice. All these results suggested that miR-4709-3p could inhibit the tumorigenesis of breast cancer cells by targeting . Finally, the underlying molecular mechanisms were investigated and we found that both NF-κB and activin signaling were involved in miR-4709-3p-related tumor inhibitory effect.