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HIF-2α activated lncRNA NEAT1 promotes hepatocellular carcinoma cell invasion and metastasis by affecting the epithelial-mesenchymal transition.

Xiaowei ZhengYiwen ZhangYujia LiuLuo FangLi LiJiao SunZongfu PanWenxiu XinPing Huang
Published in: Journal of cellular biochemistry (2017)
The aim of this study was to investigate the role of NEAT1 in hepatocellular carcinoma (HCC), and probe whether NEAT1 participate in the epithelial-mesenchymal transition (EMT) and metastasis regulated by HIF-2α. Expression of lncRNA NEAT1 was initially assessed in HCC tissues and in a series of HCC cell lines. The correlations between NEAT1 levels and HIF-2α were analyzed through plasmid vector construction. The potential underlying mechanisms of NEAT1 in HCC were performed through in vitro and in vivo functional assays. Expression of NEAT1, HIF-2α were significantly increased in HCC tissues and cell lines. Then, in vitro assays revealed that NEAT1 promotes EMT and metastasis by stimulating the inactivation of HIF-2α in HCC. An in vivo animal model also demonstrated the cancer promotion mechanism of NEAT1. In this study, we found that the NEAT1 was high expression in HCC. NEAT1 promotes tumor cell EMT, migration and invasion capacities by stimulating the activation of HIF-2α in HCC.
Keyphrases
  • epithelial mesenchymal transition
  • poor prognosis
  • endothelial cells
  • transforming growth factor
  • squamous cell carcinoma
  • high throughput
  • binding protein
  • risk assessment
  • crispr cas
  • cell therapy