MEG2 was recently found to have important functions in human cancers. However, the expression status and biological functions of MEG2 in hepatocellular carcinoma (HCC) remain unknown. In this study, we demonstrated that MEG2 expression was reduced in HCC tissues and cell lines using qRT-PCR, western blot and immunohistochemical staining. Decreased MEG2 expression predicted unfavorable clinical features and decreased overall survival and disease-free survival of HCC patients. In vitro functional assays showed that overexpression of MEG2 inhibited the cell viability, migration and invasion of HCCLM3 cells while MEG2 knockdown promoted these biological functions of Hep3B cells. Subcutaneous injection model and tail vein injection model showed that forced expression of MEG2 in HCCLM3 decreased the growth and lung metastasis of HCCLM3 cells in nude mice. Mechanically, MEG2 inhibited the EMT and AKT phosphorylation of HCC cells. The promoting effects of MEG2 knockdown on EMT, cell viability, proliferation, migration and invasion of Hep3B cells was blocked by AKT phosphorylation inhibition. In all, this study demonstrates that MEG2 inhibits the growth and metastasis of hepatocellular carcinoma by inhibiting AKT pathway.
Keywords: AKT pathway; Growth; Hepatocellular carcinoma; MEG2; Metastasis.
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