Dysregulation of N-acetyltransferase 10 (NAT10) is associated with the development of many types of tumors; however, its role in hepatocellular carcinoma (HCC) has not been fully elucidated. Here, we examined the role of NAT10 during epithelial-to-mesenchymal transition (EMT) in HCC and established its role in metastasis. We evaluated expression of NAT10 expression in four HCC cell lines and determined the effects of knockdown by siRNA or treatment with the NAT10 inhibitor, Remodelin. NAT10 was highly expressed in HCC cell lines with a mesenchymal-like phenotype (SNU387 and SNU449). Knockdown or inhibition of NAT10 resulted in diminished cell invasion and migration. Moreover, decreased levels of NAT10 were correlated with increased E-cadherin expression and down regulation of vimentin, both of which are canonical markers of EMT signaling, suggesting that NAT10-promoted metastasis may be mediated by EMT in HCC. Our data suggests that up regulation of NAT10-promoted metastasis of HCC cells may be mediated by EMT.
Keywords: E-cadherin; N-acetyltransferase 10; epithelial-to-mesenchymal transition; hepatocellular carcinoma; vimentin.