Abstract
An increasing number of studies have indicated that the deregulation of microRNAs (miRNAs) contributes to tumorigenesis and metastasis. In the present study, significant upregulation of miR-362-5p was identified in the breast cancer MDA-MB-231 and MCF7 cell lines compared with the control CCD-1095Sk cell line. The inhibition of miR-362-5p was demonstrated to significantly inhibit the cell proliferation, migration and invasion of human breast cancer MCF7 cells. In addition, the knockdown of miR-362-5p induced G1 arrest and promoted apoptosis in the breast cancer cells. Mechanistic investigations confirmed that the tumor suppressor gene CYLD is a direct target of miR-362-5p. The ectopic expression of miR-362-5p represses CYLD expression, whereas miR-362-5p inhibitor treatment induces CYLD protein expression and decreases NF-κB expression in the downstream signaling pathway. Thus, these findings may provide novel insights into the molecular mechanisms through which miR-362-5p regulates breast cancer cell proliferation, migration and invasion. This study also suggests that miR-362-5p may act as a novel potential therapeutic target for the treatment of breast cancer.