title: Isoliquiritigenin inhibits the growth of prostate cancer.
abstract: OBJECTIVE
  Isoliquiritigenin, one of the components in the root of Glycyrrhiza glabra L., is a member of the flavonoids, which are known to have an anti-tumor activity in vitro and in vivo. In this study, we investigated the anti-tumor effect of isoliquiritigenin on prostate cancer in vitro.
  
  
  METHODS
  DU145 and LNCaP prostate cancer cell lines were used as targets. We examined the effects of isoliquiritigenin on cell proliferation, cell cycle regulation and cell cycle-regulating gene expression. Further, we investigated the effects of isoliquiritigenin on the GADD153 mRNA and protein expression, and promoter activity.
  
  
  RESULTS
  Isoliquiritigenin significantly inhibited the proliferation of prostate cancer cell lines in a dose-dependent and time-dependent manner. Fluorescence-activated cell sorting (FACS) analysis indicated that isoliquiritigenin induced S and G2/M phase arrest. Isoliquiritigenin enhanced the expression of GADD153 mRNA and protein associated with cell cycle arrest. Further, isoliquiritigenin stimulated transcriptional activity of GADD153 promoter dose-dependently.
  
  
  CONCLUSIONS
  These findings suggest that isoliquiritigenin is a candidate agent for the treatment of prostate cancer and GADD153 may play an important role in isoliquiritigenin-induced cell cycle arrest and cell growth inhibition.
authors.affiliation: Department of Urology, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kyoto 602-8566, Japan. motohiro@koto.kpu-m.ac.jp
authors.forename: Motohiro
authors.initials: M
authors.lastname: Kanazawa
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Satomi
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Mizutani
authors.forename: Osamu
authors.initials: O
authors.lastname: Ukimura
authors.forename: Akihiro
authors.initials: A
authors.lastname: Kawauchi
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Sakai
authors.forename: Masaki
authors.initials: M
authors.lastname: Baba
authors.forename: Toru
authors.initials: T
authors.lastname: Okuyama
authors.forename: Hoyoku
authors.initials: H
authors.lastname: Nishino
authors.forename: Tsuneharu
authors.initials: T
authors.lastname: Miki
mesh_terms: D022762:CCAAT-Enhancer-Binding Proteins / Q000235:genetics / Q000378:metabolism; D002453:Cell Cycle / Q000187:drug effects; D002455:Cell Division; D002599:Chalcone / Q000031:analogs & derivatives* / Q000494:pharmacology*; D047188:Chalcones; D004305:Dose-Response Relationship, Drug; D005419:Flavonoids / Q000494:pharmacology*; D006035:Glycyrrhiza; D006801:Humans; D008297:Male; D010936:Plant Extracts / Q000494:pharmacology; D011401:Promoter Regions, Genetic / Q000187:drug effects; D011471:Prostatic Neoplasms / Q000378:metabolism / Q000473:pathology*; D012333:RNA, Messenger / Q000378:metabolism; D051742:Transcription Factor CHOP; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D014407:Tumor Cells, Cultured / Q000187:drug effects
chemical_list: D022762:CCAAT-Enhancer-Binding Proteins; D047188:Chalcones; C497249:DDIT3 protein, human; D005419:Flavonoids; D010936:Plant Extracts; D012333:RNA, Messenger; D014157:Transcription Factors; D051742:Transcription Factor CHOP; D002599:Chalcone; C040920:isoliquiritigenin