Hypoxia Promotes Epithelial - Mesenchymal Transition of Hepatocellular Carcinoma Cells via Inducing GLIPR-2 ExpressionReportar como inadecuado




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Glioma pathogenesis related-2 GLIPR-2 belongs to pathogenesis related-1 PR-1 family whose function remains unknown. In our previous studies, GLIPR-2 was found to be a novel potent stimulator of epithelial-to-mesenchymal transition EMT in renal fibrosis which has been classified as type 2 EMT. However, whether GLIPR-2 could induce type 3 EMT in carcinogenesis needs further investigation. In this study, we showed that GLIPR-2 was expressed in hepatocellular carcinoma HCC tissues, hypoxia could upregulate the expression of GLIPR-2 in HepG2 and PLC-PRF-5 cells in vitro, overexpression of this protein promoted migration and invasion via EMT, knockdown of GLIPR-2 attenuated migration and invasion of HepG2 and PLC-PRF-5 cells in hypoxia. Moreover, extracellular signal-regulated kinases 1 and 2 ERK1-2 are positively regulated by GLIPR-2. Taken together, we provide evidence for a hypoxia-GLIPR-2-EMT-migration and invasion axis in HCC cells and it provides novel insights into the mechanism of migration and invasion of hepatocellular carcinoma cells in hypoxia condition.



Autor: Shao-guang Huang, Le-le Zhang, Qin Niu, Gui-ming Xiang, Lin-lin Liu, Dong-neng Jiang, Fei Liu, Yi Li, Xiaoyun Pu

Fuente: http://plos.srce.hr/



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