Matrine triggers colon cancer cell apoptosis and G0/G1 cell cycle arrest via mediation of microRNA-22

Matrine (MAT) is an alkaloid in the dried roots of Sophora flavescens. The antitumor activity has been testified in colon cancer. Howbeit, the latent mechanism is still indistinct. The research probed the antitumor mechanism of MAT in colon cancer cells. MAT (0.25, 0.5, 0.75, 1, and 1.25 mM) was utilized to stimulate SW480 and SW620 cells for 24, 48, and 72 hr. Cell viability, apoptosis, cell cycle, and the correlative proteins were assessed via Cell Counting Kit-8, flow cytometry, and Western blot. microRNA-22 (miR-22) in MAT-treated or miR-22-silenced cells was estimated via real-time quantitative polymerase chain reaction. The functions of miR-22 inhibition were reassessed. Western blot was conducted for quantifying beta-catenin, MEK, and ERK. Luciferase reporter assay was done for confirming the targeting relationship between miR-22 and ERBB3 or MECOM. MAT prohibited cell viability, accelerated apoptosis, and triggered cells cycle stagnation at G0/G1 phase. Additionally, miR-22 was elevated by MAT; meanwhile, the influences of MAT were all inverted by miR-22 inhibitor. MAT enhanced the expression of miR-22, thereby obstructing Wnt/beta-catenin and MEK/ERK pathways. miR-22 had a potential to target mRNA 3'UTR of ERBB3 and MECOM. These discoveries manifested that MAT could evoke colon cancer cell apoptosis and G0/G1 cell cycle arrest via elevating miR-22. Highlights MAT restrains colon cancer cells growth; MAT triggers colon cancer cell cycle arrest at G0/G1 phase; MAT elevates miR-22 expression in colon cancer cells; MiR-22 repression inverts the functions of MAT in colon cancer cells growth and cell cycle arrest; MAT hinders Wnt/beta-catenin and MEK/ERK pathways via enhancing miR-22.