Accumulating evidence shows that
microRNA (
miRNA) is frequently associated with multiple kinds of human
cancers, including
colorectal cancer (CRC). Previous studies have shown that miR-592 play critical roles in
cancer cell biological processes. However, the function of miR-592 in CRC remains largely unknown. In the present study, we investigated the miR-592's role in cell proliferation of
colorectal cancer. MiR-592 expression was markedly down-regulated in CRC tissues and CRC cells. Overexpression of miR-592 reduced the proliferation and anchorage-independent growth of CRC cells. Furthermore, bioinformatics analysis further revealed CCND3, a putative
tumor promoter, was found to be a potential target of miR-592 in CRC. The dual-
luciferase reporter gene assay results showed that CCND3 was a direct target of miR-592. Ectopic expression of miR-592 led to down-regulation of CCND3
protein, which resulted in the down-regulation of phosphorylated
retinoblastoma (p-Rb). In functional assays, CCND3-silenced in miR-592-in-transfected SW48 cells have positive effect to suppress cell proliferation, suggesting that direct CCND3 suppression is required for miR-592-induced cell proliferation of CRC. We conclude that miR-592 can regulate CCND3 and function as a
tumor suppressor in CRC. Therefore, miR-592 represents a potential anti-onco-miR and serves as a useful therapeutic agent for
miRNA-based CRC
therapy.