Catalpol inhibits cell proliferation, invasion and migration through regulating miR-22-3p/MTA3 signalling in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is the most common type of liver malignancy with high rates of recurrence and mortality worldwide. Unfortunately, effective strategies for the management of HCC are still unsatisfactory. The aim of this investigation is to explore the effects of catalpol on HCC progression and investigated the mechanistic functions of catalpol in HCC. Catalpol significantly suppressed cell viability, caused the suppression in colony growth, decreased number of invaded and migrated HCC cells, and increased the rates of apoptotic cells and proportions of HCC cells at G0/G1 cell cycle phase. Furthermore, catalpol dramatically up-regulated miR-22-3p expression in HCC cells, and knockdown of miR-22-3p attenuated the anti-tumor effects of catalpol in HCC. Additionally, results from luciferase reporter assay demonstrated that miR-22-3p targeted the metastasis associated 1 family member 3 (MTA3) 3'untranslated region (3'UTR), and miR-22-3p down-regulated MTA3 expression in HCC cells. Overexpression of MTA3 enhanced HCC cell proliferative abilities, increased the number of invasive and migratory HCC cells, and also attenuated the anti-tumor potentials of catalpol in HCC. Catalpol suppressed HCC tumor growth and increased miR-22-3p expression, while down-regulated MTA3 expression in dissected tumor tissues from xenograft nude mice. Collectively, our results for the first time revealed the anti-tumor potentials of catalpol in HCC, and the anti-tumor effects mediated by catalpol were via modulating the miR-22-3p/MTA3 axis in HCC.