MiR-23a-3p promotes the development of colon cancer by inhibiting the expression of NDRG4.

Abstract

Previous studies have found that miR-23a-3p, a diagnostic marker for colon cancer (CC), is upregulated in primary CC from stage I/II patients. Nevertheless, the specific functions and molecular mechanisms of miR-23a-3p in colon cancer remain unclear. The expression levels of miR-23a-3p and NDRG4 were analyzed by western blot and RT‒qPCR assays. Cell viability and proliferation were measured by CCK8 and colony formation assays. Cell apoptosis was assessed by flow cytometry. Cell migration and invasion were detected by transwell assay. Target binding was detected by luciferase reporter assay. miR-23a-3p was dramatically elevated in CC tissues and cells. In HT29 and SW480 cells, downregulation of miR-23a-3p hampered cell proliferation, migration, and invasion while increasing cell apoptosis. The effects of miR-23a-3p silencing on CC progression were slowed by NDRG4 downregulation. miR-23a-3p promoted CC progression by modulating the expression of NDRG4. This study demonstrated the mechanism of miR-23a-3p in CC, which may offer a new target for CC therapy.