promotes proliferation and invasion in colorectal cancer and epithelial-mesenchymal transition.

Background: The current study aimed to investigate the effect of on the biological function of colorectal cancer (CRC) cells and its mechanism.

Methods: First, quantitative reverse transcription polymerase chain reaction (qRT-PCR) was employed for detecting the expression of , , and in surgically resected specimens from hospitalized CRC patients, CRC-adjacent normal tissues (Normal group), human normal colon epithelial cells (FHC group), and CRC cell lines (HCT116, HT29, SW480, SW620). The cell proliferation, viability, and invasion were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation assay, transwell assay in HCT116 and SW480 cells with overexpression or inhibition of . The targeting relationship between and was verified by dual-luciferase reporter assay. The expression of epithelial-mesenchymal transition (EMT) proteins (E-cadherin, vimentin, and N-cadherin) was tested by western blot.

Results: The expression level of was significantly increased in CRC tissues and cells. Overexpression of significantly increased cell proliferation rate, viability, invasion, and the EMT process, whereas knockdown of inhibited the biological performance of CRC cells. Bioinformatic analysis suggested that miR-647 was regulated by , and a dual-luciferase reporter assay further showed a targeting relationship between the two. In addition, was negatively correlated with expression in CRC.

Conclusions: Our findings suggest that promotes proliferation and invasion in CRC and EMT. These effects of c may be achieved by negatively regulating miR-62.