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MicroRNAs are small non-coding RNAs that are implicated in various biological processes.  Hsa-miR-6165  (miR-6165), located in the  p75NTR  gene, is known to induce apoptosis in human cell lines, but its mechanism of action is not fully understood yet. Here, we predicted the insulin-like growth factor 1 receptor ( IGF-1R ) gene as a  bona fide  target for miR-6165. The overexpression of miR-6165 in SW480 cells resulted in significant downregulation of IGF-1R expression as detected by real time quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA). Also, it resulted in reduced transcript levels of  AKT2 ,  AKT3 ,  PI3KR3 ,  PI3KR5 ,  CCND1 ,  c-MYC  and  P21  genes detected by RT-qPCR analysis. In addition, a direct interaction between miR-6165 and a 3′UTR sequence of the  IGF-1R  gene was verified through a dual luciferase assay. Furthermore,  miR-6165  and  IGF-1R  showed opposite patterns of expression during the neural differentiation process of NT2 cells. Annexin V analysis and MTT assay showed that miR-6165 overexpression was followed by increased apoptosis and reduced the viability rate of SW480 cells. Moreover, a lower expression level of miR-6165 was detected in high-grade colorectal tumors compared with low-grade tumors. Taken together, the results of our study suggest a tumor suppressive role of miR-6165 in colorectal cancer, which seems to take place by regulating  IGF-1R  gene expression.

Hsa-miR-6165 downregulates insulin-like growth factor-1 receptor (IGF-1R) expression and enhances apoptosis in SW480 cells