| Literature DB >> 29309535 |
Chenyue Zhang1,2, Haiyong Wang1,3, Zhiao Chen4, Liping Zhuang1,2, Litao Xu1,2, Zhouyu Ning1,2, Zhenfeng Zhu1,2, Peng Wang1,2, Zhiqiang Meng1,2.
Abstract
Carbonic anhydrase 2 (CA2) plays vital role in the regulation of ion transport and pH balance and is involved in many biological processes; however, its role in cancer remains obscure. In this study, we identified a novel function of CA2 in facilitating hepatocellular carcinoma (HCC) metastasis. CA2 expression was elevated in Na+-K+-ATPase α1 (ATP1A1)-downregulated HCC cells and was inversely correlated with that of ATP1A1 in HCC. ATP1A1 acted as an oncoprotein whereas CA2 overexpression inhibited cell migration and invasion by reversing epithelial-mesenchymal transition (EMT) in HCC. CA2 downregulation promoted HCC metastasis and invasion whereas ATP1A1 downregulation inhibited HCC metastasis. Because of the opposing effects of CA2 and ATP1A1 in HCC, we examined the role of their correlation in HCC metastasis. CA2 attenuated ATP1A1-triggered tumor growth in vivo and ATP1A1-induced metastasis in vitro. Taken together, the present results suggest that CA2 serves as a suppressor of HCC metastasis and EMT and is correlated with favorable overall survival (OS) in HCC patients.Entities:
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Year: 2018 PMID： 29309535 DOI： 10.1093/carcin/bgx148
Source DB: PubMed Journal: Carcinogenesis ISSN： 0143-3334 Impact factor: 4.944