MiR-92a promotes the invasion and migration of colorectal cancer by targeting RECK

The up regulation of miR-92a in human cancer happens frequently, and is related to an increase of metastasis and decreased survival. However, its functions in colorectal cancer (CRC) are largely unknown. This study aimed to investigate the regulatory effect of miR-92a on cell invasion and migration in colorectal cancer (CRC). A total of 158 patients with CRC were included, and in situ hybridization was used to predict the expression of miR-92a in the paraffin sections from the patients. Quantitative reverse transcription PCR was used to detect the expression of miR-92a and its target gene. Protein levels were determined by western blotting. Luciferase assays confirmed the direct target of miR-92a. Furthermore, cell invasion and migration were detected using Transwell and wound healing assays. The expression level of miR-92a in tumor tissues was upregulated compared with that of paired normal tissues and negatively correlated with the RECK protein level. The 3-year disease-free survival (DFS) and overall survival (OS) rates of miR-92a expression in the high group were significantly lower than those in the miR-92a-low group. The RECK 3'-UTR reporter activity assay suggested that the RECK gene was a direct target of miR-92a. After transfection of the miR-92a-mimic, the miR-92a levels were increased in HCT116 and SW620 cell lines, while the protein expression of RECK was decreased instead of the mRNA level, along with downregulation of matrix metalloproteinase (MMP) protein expression. Conversely, after transfection with miR-92a-inhibitor, the opposite trend was achieved. In conclusion, miR-92a promotes the invasion and migration of CRC through the RECK-MMP signaling pathway, and the upregulation of miR-92a was associated with poor long-term prognosis in CRC.