Knockdown of miR-92a suppresses the stemness of colorectal cancer cells via mediating SOCS3

MiRNAs (microRNAs) participate in colorectal cancer (CRC) progression and act as potential biomarkers for CRC prognosis. In this study, we investigated the mechanisms of microRNA-92a (miR-92a) in CRC. Expressions of miR-92a and SOCS3 (Suppressor Of Cytokine Signaling 3) were investigated by qRT-PCR in CRC cell lines and 30 cases of CRC. The self-renewal capacity and proliferation of CRC stem cells were estimated by the sphere formation assay, EdU staining, and Flow cytometry analysis. Moreover, the interplay between miR-92a and SOCS3 in CRC cells was validated by luciferase reporter experiments. MiR-92a was found to be remarkably increased while SOCS3 was significantly downregulated in CRC tissues. Inhibition of miR-92a or SOCS3 attenuated the sphere formation capacity, decreased expressions of stemness-related proteins, and inhibited the proliferation of cancer stem-like cells. Knockdown of SOCS3 reversed the repressive impacts of miR-92a inhibitors on self-renewal and growth of CRC cancer stem cells. This study suggested that miR-92a functions as an oncogene of CRC through mediating the stemness of colorectal cancer cells by directly binding and repressing SOCS3.

Automated summary

This study investigates the role of miR-92a in colorectal cancer (CRC). It is found that miR-92a functions as an oncogene by directly binding and repressing SOCS3, resulting in the regulation of stemness and proliferation of CRC cells.