title: Proliferative response of human prostate cancer cell to hormone inhibited by androgen receptor antisense RNA.
abstract: BACKGROUND
  The failure of endocrine treatment for advanced prostate cancer might be related to aberrant activation of androgen receptor (AR). Prostate cancer cell line LNCaP contains AR that can be activated by androgen, estrogen and progesterone. This study was set to investigate the effects of antisense AR RNA on growth of LNCaP cultured in medium containing varied concentrations of R1881, 17beta-estradiol, and progesterone, respectively.
  
  
  METHODS
  LNCaP cells transfected with antisense AR RNA retroviral vector pL-AR-SN were designated as LNCaPas-AR. LNCaP cells containing empty vector pLXSN served as LNCaPNeo. LNCaP and LNCaPNeo were taken as controls. In vitro cell growth assay, proliferative cells of LNCaP and tranfected LNCaPs were counted by typan staining when they cultured with synthetic androgen R1881, 17beta-estradiol, and progesterone, respectively.
  
  
  RESULTS
  Growth of LNCaPas-AR was inhibited significantly (P < 0.05) compared with that of LNCaP and LNCaPNeo at 1 nmol/L R1881, 10 nmol/L 17beta-estradiol, and 1 nmol/L progesterone, respectively. No difference was seen between LNCaP and LNCaPNeo (P > 0.05). Microscopic observation showed that LNCaP and LNCaPNeo cells grew well, but only few LNCaPas-AR cells were alive.
  
  
  CONCLUSIONS
  Our observations indicate that antisense AR RNA retroviral vector pL-AR-SN could change androgen-independent characteristics of LNCaP cells, which might shed some novel insights into the treatment of androgen-independent prostate cancer.
authors.affiliation: Department of Urology, Daping Hospital, Third Military Medical University, Chongqing 400042, China. a68819049@cta.cq.cn
authors.forename: Jun
authors.initials: J
authors.lastname: Jiang
authors.forename: Luo-fu
authors.initials: LF
authors.lastname: Wang
authors.forename: Yu-hua
authors.initials: YH
authors.lastname: Fang
authors.forename: Feng-shuo
authors.initials: FS
authors.lastname: Jin
authors.forename: Wen-sheng
authors.initials: WS
authors.lastname: Jin
mesh_terms: D059002:Androgen Receptor Antagonists; D002455:Cell Division / Q000187:drug effects; D045744:Cell Line, Tumor; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000494:pharmacology; D006801:Humans; D008297:Male; D015741:Metribolone / Q000037:antagonists & inhibitors / Q000494:pharmacology; D011374:Progesterone / Q000037:antagonists & inhibitors / Q000494:pharmacology; D011471:Prostatic Neoplasms / Q000473:pathology / Q000628:therapy*; D016372:RNA, Antisense / Q000627:therapeutic use*; D011944:Receptors, Androgen / Q000235:genetics
chemical_list: D059002:Androgen Receptor Antagonists; D016372:RNA, Antisense; D011944:Receptors, Androgen; D015741:Metribolone; D011374:Progesterone; D004958:Estradiol