MiR-612 Suppresses the Proliferation and Migration of Breast Cancer Cells and Induces their Apoptosis Through the AKT/ERK Signaling Cascade
Abstract MicroRNAs (miRs) as non-coding RNAs have been generating widespread interest in cancer diagnosis and treatment. Among the previously studied miRs, miR-612 has been addressed to have a tumor suppressor function in all types of the studied cancers except esophageal squamous cell carcinoma. Despite this interest, the exact function of miR-612 in breast cancer (BC) remains elusive. Within the framework of these criteria, we tried to study the role of miR-612 in BC development. The human BC cell lines, MDA-MB-231 and MDA-MB-468 were transfected with miR-612. The effects of miR-612 replacement on viability, migration, invasion, cell cycle, apoptosis, and colony formation were studied in vitro. Furthermore, the protein expression of AKT and ERK were evaluated by Western blotting analysis. The results indicated that miR-612 decreased cell viability, migration, invasion, and colony formation of BC cells. Moreover, apoptosis was augmented, and thus cell cycle arrest was induced. Also, miR-612 decreased the expression and phosphorylation of proteins of the AKT/ERK signaling pathway. We suggest that miR-612-related stimulatory effects on apoptosis and its inhibitory impacts on proliferation and migration of BC cells mediates partly by suppressing the AKT/ERK signaling pathway.