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

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.