title: Effect of AT1R knockdown on ishikawa cell proliferation induced by estrogen.
abstract: OBJECTIVE
  This study aimed to study the effects of angiotensin receptor (AT1R) on proliferation, cell cycle progression, and apoptosis of estrogen-induced ishikawa cell by the transfection of AT1R-siRNA.
  
  
  METHODS
  Immunofluorescence method was used to detect AT1R in ishikawa cell. Western blot was used to detect the expression of AT1R protein in ishikawa cell before and after the transfection of AT1R-siRNA. MTT method was used to test the cell proliferation of estrogen-induced ishikawa cell before and after the transfection. Western blot was used to detect the expression of extracellular regulated protein kinase1/2(ERK1/2).
  
  
  RESULTS
  The result of immunofluorescence shows that AT1R was expressed in ishikawa cell. The expression of AT1R protein was inhibited obviously by 72 h after the transfection of AT1R-siRNA. The results of MTT show that estrogen could induce the cell proliferation of ishikawa cell. The expression of ERK1/2 was down-regulated after the transfection of AT1R-siRNA.
  
  
  CONCLUSIONS
  AT1R can promote the cell proliferation of estrogen-induced ishikawa cell. The possible mechanism may be down-regulating the expression of ERK1/2 protein.
authors.affiliation: Department of Obstetrics and Gynecology, Shengjing Hospital, China Medical University, Shen Yang 110004, China. Yangq@sj-hospital.org
authors.forename: Qing
authors.initials: Q
authors.lastname: Yang
authors.forename: Qing
authors.initials: Q
authors.lastname: Su
authors.forename: Guangwei
authors.initials: G
authors.lastname: Wang
authors.forename: Fangfang
authors.initials: F
authors.lastname: Bi
authors.forename: Rina
authors.initials: R
authors.lastname: Sa
mesh_terms: D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D015536:Down-Regulation; D016889:Endometrial Neoplasms / Q000188:drug therapy / Q000235:genetics; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D055785:Gene Knockdown Techniques / Q000379:methods; D006801:Humans; D019950:Mitogen-Activated Protein Kinase 1 / Q000096:biosynthesis; D048052:Mitogen-Activated Protein Kinase 3 / Q000096:biosynthesis; D044140:Receptor, Angiotensin, Type 1 / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D004967:Estrogens; D044140:Receptor, Angiotensin, Type 1; C535150:MAPK1 protein, human; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3