miR-23b is a negative regulator of tumor suppressing PTPRG in colorectal cancer

Colorectal cancer (CRC) is among top most common cancers with high mortality rate and major health issue yet to resolve across the globe. miR-23b is an oncogene in many cancers including CRC. The route of involvement of miR-23b in the regulation of CRC is still unclear. Study explored bioregulatory mechanism of miR-23b against CRC involving in vitro and animal model experimentation via experimentation involving ki67 immunohistochemistry, CCK8, EDU, and Transwell cell migration. The bioinformatic studies were employed to predict miR-23b target tumor suppressor PTPRG while the luciferase reporter gene assay was used to find the binding capabilities of miR-23b to the 3'-UTR of PTPRG. The changes in the expression of miR-23b were found in three CRC cell lines including SW480, HT29, and Caco2, and their correlation with PTPRG protein were assessed through western blot and RT-PCR. Moreover, the association of PTPRG gene in the SW480 cell on CRC by CCK8, EDU, and Transwell cell migration assay. Furthermore, we also detected the PTPRG protein levels in clinical samples of the tissues. Afterwards, the regulatory involvement PTPRG through miR-23b was studied by means of co-overexpression in both animals based and cell-based studies. CRC growth is associated with miR-23b and directly targets the PTPRG in CRC cells. PTPRG may restrict the cell proliferation and migration and can restore the miR-23b mediated CRC growth. MiR-23b is directly linked with the CRC development via PTPRG restriction suggesting miR-23b as novel therapeutic target against CRC.