MicroRNA-582 promotes tumorigenesis by targeting phosphatase and tensin homologue in colorectal cancer

Abstract

A number of studies have implicated that a class of non-coding RNAs named microRNAs (miRNAs or miRs) is associated with tumorigenesis and have identified miRNAs as promising targets for pharmaceutical intervention. Recently, the deregulated expression of miR-582 in tumor cells has been reported. However, the exact function of miR-582 in colorectal cancer (CRC) remains largely unknown. In thi study, we demonstrate that miR-582 is extensively upregulated in CRC tissues and cell lines. The overexpression of miR-582 significantly enhanced the proliferation and migration ability of the CRC cells. However, the use of a specific miR-582 inhibitor counteracted these effects. miR-582 may also play an oncogenic role by promoting tumor growth in vivo. Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) was identified as a putative target of miR-582; transfection of the cells with a lentivirus with miR-582 mimics substantially decreased both the mRNA and protein levels of PTEN. The restoration of PTEN expression in the CRC cells reversed the adverse effects of miR-582. Our findings therefore indicate that miR-582 promotes CRC progression by decreasing PTEN expression. These findings may also imply that miR-582 may be a target for therapeutic intervention in patients with CRC.