NAT10的上调通过上皮-间质转化促进肝癌细胞转移。
Up regulation of NAT10 promotes metastasis of hepatocellular carcinoma cells through epithelial-to-mesenchymal transition.
作者信息
Ma Rui, Chen Jiang, Jiang Shaojie, Lin Shuang, Zhang Xiuming, Liang Xiao
机构信息
Department of Surgery, Zhejiang University Hospital, Zhejiang University Hangzhou 310027, Zhejiang, China.
Department of General Surgery, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University Hangzhou 310016, Zhejiang, China.
出版信息
Am J Transl Res. 2016 Oct 15;8(10):4215-4223. eCollection 2016.
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.
N-乙酰转移酶10（NAT10）的失调与多种肿瘤的发生发展相关；然而，其在肝细胞癌（HCC）中的作用尚未完全阐明。在此，我们研究了NAT10在HCC上皮-间质转化（EMT）过程中的作用，并确定了其在转移中的作用。我们评估了NAT10在四种HCC细胞系中的表达情况，并通过小干扰RNA（siRNA）敲低或使用NAT10抑制剂Remodelin处理来确定其影响。NAT10在具有间充质样表型的HCC细胞系（SNU387和SNU449）中高表达。敲低或抑制NAT10会导致细胞侵袭和迁移能力减弱。此外，NAT10水平降低与E-钙黏蛋白表达增加及波形蛋白下调相关，这两者都是EMT信号通路的典型标志物，表明NAT10促进的转移可能由HCC中的EMT介导。我们的数据表明，NAT10上调促进HCC细胞转移可能由EMT介导。
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