MiR-483 Promotes Colorectal Cancer Cell Biological Progression by Directly Targeting NDRG2 through Regulation of the PI3K/AKT Signaling Pathway and Epithelial-to-Mesenchymal Transition

BACKGROUND: Colorectal cancer is the third frequent tumor in the whole world. MiR-483, located at the 11p15.5 locus, acts as an oncogene in multiple tumors. The purpose of this study is to explore the important roles of miR-483 in colorectal cancer. MATERIALS AND METHODS: RT-qPCR and western blot were applied to calculate the mRNA levels of miR-483 and genes. The Kaplan–Meier method was conducted to calculate the survival of patients with colorectal cancer. The proliferation and invasive abilities were measured by Methyl Thiazolyl Tetrazolium (MTT) and transwell assays. RESULTS: MiR-483 was upregulated in colorectal cancer tissues, and the upregulation of miR-483 predicted poor prognosis of colorectal cancer patients. NDRG2 was a target gene of miR-483 in colorectal cancer. Furthermore, miR-483 has been reported to promote colorectal cancer cell proliferation and invasion through targeting NDRG2 by the PI3K/AKT pathway and epithelial-to-mesenchymal transition (EMT). In addition, the overexpression of miR-483 promoted xenograft growth of LOVO cells. CONCLUSION: MiR-483 promoted cell proliferation through the NDRG2/PI3K/AKT pathway and invasion-mediated EMT in colorectal cancer. In view of the multiple mechanisms of molecular immunotherapy, it is necessary to further study the relationship between miR-483 and colorectal cancer, so as to find a more direct and effective treatment method to prevent colorectal cancer.