title: An upstream estrogen response element linked to exogenous p53 tumor suppressor gene expression differentiates effects of the codon 72 polymorphism.
abstract: 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.
authors.affiliation: Department of Obstetrics and Gynecology, Osaka City University Graduate School of Medicine, Osaka, Japan. kenhonda@med.osaka-cu.ac.jp
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Honda
authors.forename: Koji
authors.initials: K
authors.lastname: Kajitani
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Nobeyama
authors.forename: Yukimi
authors.initials: Y
authors.lastname: Kira
authors.forename: Yoriko
authors.initials: Y
authors.lastname: Yabunaka
authors.forename: Mika
authors.initials: M
authors.lastname: Egami
authors.forename: Xu
authors.initials: X
authors.lastname: Zhi
authors.forename: Takeshi
authors.initials: T
authors.lastname: Fukuda
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Yoshida
authors.forename: Yoshinari
authors.initials: Y
authors.lastname: Matsumoto
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Ichimura
authors.forename: Tomoyo
authors.initials: T
authors.lastname: Yaui
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Sumi
authors.forename: Osamu
authors.initials: O
authors.lastname: Ishiko
mesh_terms: D001120:Arginine / Q000235:genetics; D002453:Cell Cycle / Q000235:genetics; D045744:Cell Line, Tumor; D003062:Codon; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000096:biosynthesis / Q000235:genetics; D016889:Endometrial Neoplasms / Q000235:genetics / Q000378:metabolism; D004967:Estrogens / Q000235:genetics*; D005260:Female; D015870:Gene Expression; D016158:Genes, p53; D006801:Humans; D011110:Polymorphism, Genetic; D011392:Proline / Q000235:genetics; D011960:Receptors, Estrogen / Q000096:biosynthesis / Q000235:genetics; D020218:Response Elements; D014162:Transfection / Q000379:methods; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis / Q000235:genetics*
chemical_list: D003062:Codon; D050759:Cyclin-Dependent Kinase Inhibitor p21; D004967:Estrogens; D011960:Receptors, Estrogen; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; D001120:Arginine; D011392:Proline