Abstract:
Objective To explore the role and mechanism of maternally expressed gene 3 (MEG3) in the development of hepatocellular carcinoma.
Methods The expression of MEG3 in normal cells and HL-7702 cells was detected with quantitative real-time reverse transcription PCR (qRT-PCR). Cell proliferation was assessed with Cell Counting Kit-8 (CCK8) assay. Cell apoptosis was tested with flow cytometry. The expression of vascular endothelial growth factor alpha (VEGFA) and its receptor (vascular endothelial growth factor receptor 1, VEFGR1) were measured with Western blot.
Results Compared with that of normal hepatic cell line HL-7702, the expression of MEG3 was decreased in hepatoma carcinoma cell lines MHCC97L, SMMC7721, MHCC97H, and HepG2 (P < 0.01). Compared with those of the control cells transfected with LV-scramble, the cell proliferation was attenuated in LV-MEG3-transfected SMMC7721 cells (from 5.8 ± 0.4 to 3.1 ± 0.3 folds) and MHCC97 cells (from 6.4 ± 0.5 to 3.4 ± 0.3 folds), but the cell apoptosis rate was increased (from 2.8 ± 0.4% to 12.4 ± 0.6% for SMMC7721 cells and from 2.2 ± 0.4% to 13.5 ± 0.5% for MHCC97H cells); moreover, the expressions of VEGFA and VEGFR1 were significantly inhibited in LV-MEG3-transfected SMMC7721 and MHCC97 cells (both P < 0.01).
Conclusion Long non-coding RNA MEG33 inhibits cell proliferation and promotes cell apoptosis in hepatocellular carcinoma cells and the effects may associate with the down regulation of VEGFA and VEFGR1.
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