microRNA‑630 promotes cell proliferation and inhibits apoptosis in the HCT116 human colorectal cancer cell line.

Dysregulation of microRNAs (miRNAs) in colorectal cancer provides important opportunities for the development of future miRNA‑based therapies. The present study aimed to assess the role of miRNA‑630 (miR‑630) expression in colorectal cancer. HCT116 human colorectal cancer cells were transfected with miR‑630 inhibitor, mimic or control miRNA, and the effects of miR‑630 dysregulation on cell viability, proliferation and apoptosis were analyzed using MTT and bromodeoxyuridine assays, and an annexin V‑fluorescein isothiocyanate cell apoptosis kit, respectively. In addition, the changes in the protein expression of proliferation‑associated and AKT signaling pathway proteins were analyzed by western blot analysis. The results of the present study demonstrated that overexpression of miR‑630 significantly promoted HCT116 cell proliferation however inhibited apoptosis. Furthermore, miR‑630 overexpression reduced the protein expression of p27, BCL2‑associated X apoptosis regulator, procaspase‑3 and active caspase‑3, and increased the levels of phosphorylated‑AKT and BCL2 apoptosis regulator. The suppression of miR‑630 led to the opposite results. In conclusion, the present findings suggested that miR‑630 may function as an oncogenic miRNA in colorectal cancer, and may promote cellular proliferation and inhibit apoptosis, through the regulation of the expression of p27 and the AKT signaling pathway. The present study suggested that the inhibition of miR‑630 may have potential as an alternative therapeutic strategy for the treatment of patients with colorectal cancer. [ABSTRACT FROM AUTHOR]