Abstract
Meningioma-associated protein 30 (MAC30) has been recently identified as a new tumor-associated protein that is implicated in multiple tumor types. However, the role of MAC30 in hepatocellular carcinoma (HCC) has not been studied. In the current study, we explored the expression, biological function and underlying mechanism of MAC30 in HCC. We found that MAC30 expression was significantly elevated in HCC tissues and cell lines. Functional in vitro assays demonstrated that the knockdown of MAC30 inhibited the proliferation and invasion of HCC cells, while MAC30 overexpression facilitated these biological behaviors. Moreover, the knockdown of MAC30 decreased glycogen synthase kinase (GSK)-3β phosphorylation level and β-catenin expression, leading to the inactivation of Wnt/β-catenin signaling in HCC cells. The inhibition of GSK-3β or reactivation Wnt/β-catenin signaling markedly reversed MAC30 knockdown-mediated inhibitory effects on the proliferation and invasion of HCC cells. Notably, the inhibition of Wnt/β-catenin signaling abrogated the MAC30-evoked oncogenic role in HCC cells. In addition, the knockdown of MAC30 impeded tumor formation and the growth rate of HCC cells in vivo. Taken together, our data recognized MAC30 as a potential tumor-promotion factor in HCC, which accelerated the proliferation and invasion of HCC through the up-regulation of Wnt/β-catenin signaling. Our study suggests MAC30 as a potential anticancer target for HCC.