Hepatocyte Nuclear Factor 4α Inhibits Expression of Vascular Endothelial Growth Factor in Human Hepatocellular Carcinoma Cell Lines and Tube Formation of Human Umbilical Vein Endothelial Cell
10.3969/j.issn.1008-7125.2017.04.003
- VernacularTitle:肝细胞核因子4α抑制人肝癌细胞株血管内皮生长因子表达和人脐静脉内皮细胞小管形成
- Author:
Haitian WANG
;
Yong ZHANG
;
Ning WU
;
Jin ZHOU
;
Hualian HANG
;
Yong MA
;
Jianmin BIAN
- Keywords:
Hepatocyte Nuclear Factor 4-alpha;
Carcinoma;
Hepatocellular;
Vascular Endothelial Growth Factors;
Human Umbilical Vein Endothelial Cells
- From:
Chinese Journal of Gastroenterology
2017;22(4):203-207
- CountryChina
- Language:Chinese
-
Abstract:
Background: Hepatocyte nuclear factor 4α (HNF4α) plays an important role in the development of liver,and studies demonstrate that it is correlated with the pathogenesis of hepatocellular carcinoma (HCC).However,the regulatory effect of HNF4α on expression of vascular endothelial growth factor (VEGF) in human HCC cell lines and tube formation of human umbilical vein endothelial cell (HUVEC) is not yet clear.Aims: To investigate the effect of HNF4α on expression of VEGF in human HCC cell lines and tube formation of HUVEC.Methods: Lentiviral vector overexpressed HNF4α was constructed,and then transfected into HepG2 and SMMC-7721 cells (experimental group),cells transfected with lentiviral blank vector and cells without transfection were served as negative control group and blank control group,respectively.The mRNA and protein expressions of HNF4α,VEGF were detected by qRT-PCR and Western blotting,respectively.The conditioned media of HepG2 and SMMC-7721 cells were co-cultured with HUVEC,and number of HUVEC tube formation was measured.Results: HepG2 and SMMC-7721 cells with stable overexpression of HNF4α were successfully established.Compared with negative control group and blank control group,mRNA and protein expressions of VEGF in experimental group were significantly decreased (P＜0.05),and number of HUVEC tube formation was significantly decreased (P＜0.05).Conclusions: HNF4α can significantly inhibit the expression of VEGF in HepG2 and SMMC-7721 cells and tube formation of HUVEC.
