NDLI: VEGF expression and its reguration by p53 gene transfection in endometrial carcinoma cells

Content Provider	Springer Nature Link
Author	Fujisawa, T. Watanabe, J. Kamata, Y. Hamano, M. Hata, H. Kuramoto, H.
Copyright Year	2003
Abstract	Vascular endothelial growth factor (VEGF) that activates endothelial cell growth induces angiogenesis, which is indispensable to tumor igenesis and tumor progression. On the other hand, tumor suppressor gene p53 has been considered to regulate VEGF expression, but the detailed relationship between them remains unclear. In this study, we aimed to study VEGF expression in endometrial carcinoma cells and the effect of p53 gene transfection on VEGF expression using p53-mutated endometrial carcinoma cell line. HEC-50B. Immunoblotting for detecting VEGF protein, p53 protein and β-actin was performed using 11 endornetrial carcinoma cell lines. Levels of VEGF in the cultured media were measured by Enzyme immunoassay(EIA). Tmsfection of wild p53 gene was carried out by SuperFect method in HEG50B cells, which had mutant p53 gene and did not express p53 protein. The results of immunoblotting were analyzed by NIH image and expressed as values. The results of EIA were expressed as the relative value. The VEGF value was 0.8±0.3 (n=6) in p53-wild group, whereas in p53-rnutant group it was 1.6±0.8 (n=5). VEGF expression was correlated significantly with p53 status (P<0.05). VEGF levels in p53 gene-msfected cells and the conditioned medium were decreased in 48 hours after p53 gene transfection. VEGF expression was down-regulated by p53 in endometrial carcinoma cells.
Starting Page	47
Ending Page	54
Page Count	8
File Format	PDF
ISSN	09147470
Journal	Human Cell
Volume Number	16
Issue Number	1
e-ISSN	17490774
Language	English
Publisher	Springer-Verlag
Publisher Date	2012-08-03
Publisher Place	Tokyo
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	endometrial cancer VEGF p53 gene transfection HEC-50 Cell Biology Embryology Oncology Stem Cells Reproductive Medicine Cell Culture
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Cancer Research

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