Reference - Detail
|Author||Honda K, Kajitani K, Nobeyama H, Kira Y, Yabunaka Y, Egami M, Zhi X, Fukuda T, Yoshida H, Matsumoto Y, Ichimura T, Yaui T, Sumi T, Ishiko O.|
|Title||An upstream estrogen response element linked to exogenous p53 tumor suppressor gene expression differentiates effects of the codon 72 polymorphism.|
|Journal||Asian Pac J Cancer Prev|
The objective of this study was to assess the effects of an upstream estrogen response element (ERE) on exogenous p53 tumor suppressor gene with a codon 72 polymorphism about which there have been controversial reports in relation to cancer risk. The p53 gene (bases 166-1143 from start codon) with the codon 72 polymorphism, inserted into the pIRES-hrGFP II plasmid with or without upstream ERE, were transfected into HHUA endometrial cancer cells expressing the estrogen receptor. The ERE-linked p53 gene with the proline variant at codon 72 showed lower transfection rates than the gene without ERE or with the arginine variant at codon 72. p21 expression was significantly higher in HHUA cells transfected with the proline variant gene than in those transfected with the arginine variant gene. We consider that the presence of an upstream ERE promotes the transcriptional effects of the exogenous p53 gene with the proline variant, which strengthens the expression of p21, and results in lower transfection rates through cell cycle inhibition.
|MeSH||Arginine / genetics Cell Cycle / genetics Cell Line, Tumor Codon* Cyclin-Dependent Kinase Inhibitor p21 / biosynthesis Cyclin-Dependent Kinase Inhibitor p21 / genetics Endometrial Neoplasms / genetics Endometrial Neoplasms / metabolism Estrogens / genetics* Female Gene Expression Genes, p53 Humans Polymorphism, Genetic Proline / genetics Receptors, Estrogen / biosynthesis Receptors, Estrogen / genetics Response Elements* Transfection / methods Tumor Suppressor Protein p53 / biosynthesis Tumor Suppressor Protein p53 / genetics*|
|Human and Animal Cells||HHUA(RCB0658)|