Recently, it has been reported that miR-324-3p participates in regulation of the
carcinogenesis and
tumor progression in various
cancers. However, the expression and function of miR-324-3p in
hepatocellular carcinoma (HCC) remain unclear. In the current study, miR-324-3p expression was significantly up-regulated in HCC tissues and cell lines. HCC patients with high miR-324-3p level showed poor prognostic features and shorter overall survival and disease-free survival. And in vitro and in vivo experiments revealed that miR-324-3p promoted cell viability, colony formation, proliferation and cell cycle progression of HCC cells. Further studies demonstrated that miR-324-3p could directly target DACT1 (dishevelled binding antagonist of
beta catenin 1) and negatively regulated its expression in HCC cells. And rescue experiments revealed that DACT1 could reverse the effects of miR-324-3p on HCC cells. Furthermore, the accumulation of both cytoplasmic and nuclear β-
catenin as well as its downstream targets including c-Myc and
cyclin D1 could be positively regulated by miR-324-3p. The regulatory effects of miR-324-3p on β-
catenin, c-Myc and
cyclin D1 levels could be reversed by DACT1. Overall, we concluded that miR-324-3p could promote
tumor growth through targeting DACT1 and activation of Wnt/β-
catenin pathway in HCC. MiR-324-3p may be a ponderable and promising therapeutic target for HCC.