miR-217 regulates tumor growth and apoptosis by targeting the MAPK signaling pathway in colorectal cancer.

MicroRNA (miR)-217 has been reported to participate in carcinogenesis and tumor progression in several cancers; however, its expression and biological functions in colorectal cancer (CRC) are still unclear. The present study demonstrated that miR-217 expression was significantly higher in matched adjacent noncancerous tissues than in CRC tissues (P<0.001). In addition, it was observed that low-grade CRC exhibited greater expression of miR-217 compared with high-grade CRC (P<0.05). Kaplan-Meier survival and Cox regression analyses revealed that overall survival rates were significantly poorer in the low-expression group relative to the high-expression group (P<0.005). Next, a potential miR-217 target, mitogen-activated protein kinase (MAPK) 1, was identified. Upregulation of miR-217 could significantly downregulate MAPK1 expression. CRC cells overexpressing miR-217 exhibited cell growth inhibition by significant enhancement of apoptosis . The present study further investigated the MAPK signaling pathway to verify the mechanisms, and revealed that KRAS and Raf-1 expression was downregulated in miR-217-overexpressing RKO cells. Taken together, our results revealed that miR-217 inhibits tumor growth and enhances apoptosis in CRC, and that this is associated with the downregulation of MAPK signaling. These results indicate that miR-217 is a promising therapeutic target for the treatment of CRC.