miR-124-3p inhibits CRC proliferation, migration, and invasion by targeting ITGB1.

Colorectal cancer (CRC) was the third most common cause of mortality associated with cancer globally. miR-124-3p has been widely acknowledged for its pivotal role as a tumor suppressor in various malignancies. In this study, we aimed to investigate the specific functions and underlying mechanisms of miR-124-3p in CRC cell proliferation, migration and invasion. A comprehensive set of assays, including CCK-8, colony formation, wound healing assays, flow cytometry, RT-qPCR and Western blotting, were conducted to assess the impact of miR-124-3p expression on CRC cell growth. Our investigations into miR-124-3p and its potential target gene ITGB1 were facilitated through bioinformatics analysis and dual-luciferase reporter assays. To further solidify our findings, rescue experiments were executed to validate the role of miR-124-3p in regulating the proliferation, migration, and apoptosis of CRC cells, genes involving Wnt/β-catenin signaling pathway were also detected. Our study revealed that the overexpression of miR-124-3p significantly suppressed both the proliferation and migratory capabilities of CRC cells, while its downregulation had the opposite effect. Notably, ITGB1 was identified as a putative target gene of miR-124-3p, exhibiting an inverse correlation with the expression levels of miR-124-3p. Moreover, the overexpression of ITGB1 was able to abrogate the inhibitory effects exerted by miR-124-3p overexpression on CRC cell proliferation, migration, and Wnt1/β-catenin protein levels. Our results reveal that miR-124-3p targets ITGB1 to regulate CRC cell proliferation and migration may be associated with the Wnt/β-catenin signaling pathway. These findings provide that a miR-124-3p/ITGB1 axis may be a potential target for the treatment of CRC.