MiR-324-3p promotes tumor growth through targeting DACT1 and activation of Wnt/β-catenin pathway in hepatocellular carcinoma
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Hang Tuo1,*, Yufeng Wang1,*, Liang Wang1, Bowen Yao1, Qing Li1, Cong Wang1, Zhikui Liu1, Shaoshan Han1, Guozhi Yin1, Kangsheng Tu1 and Qingguang Liu1
1Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi Province 710061, China
*These authors contributed equally to this work
Qingguang Liu, email: [email protected]
Kangsheng Tu, email: [email protected]
Keywords: hepatocellular carcinoma, miR-324-3p, DACT1, proliferation, Wnt/β-catenin pathway
Received: June 22, 2017 Accepted: July 26, 2017 Published: August 07, 2017
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.
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