title: Anticancer effects of (-)-epigallocatechin-3-gallate on ovarian carcinoma cell lines.
abstract: OBJECTIVE
  A constituent of green tea, (-)-epigallocatechin-3-gallate (EGCG), has been known to possess anti-cancer properties. In this study, we investigated the time-course anticancer effects of EGCG on human ovarian cancer cells to provide insights into the molecular-level understanding of growth suppression mechanism involved in EGCG-mediated apoptosis and cell cycle arrest.
  
  
  METHODS
  Three human ovarian cancer cell lines (p53 negative, SKOV-3 cells; mutant type p53, OVCAR-3 cells; and wild type p53, PA-1 cells) were used. The effect of EGCG treatment was studied via cell count assay, cell cycle analysis, FACS, Western blot, and macroarray assay.
  
  
  RESULTS
  EGCG exerts a significant role in suppressing ovarian cancer cell growth. Also, EGCG showed growth inhibitory effects in each cell line in a dose-dependent fashion and induced apoptosis and cell cycle arrest. The cell cycle was arrested at the G(1) phase by EGCG in SKOV-3 and OVCAR-3 cells. In contrast, the cell cycle was arrested in the G(1)/S phase arrest in PA-1 cells. EGCG differentially regulated the expression of genes and proteins (Bax, p21, Retinoblastoma, cyclin D1, CDK4, Bcl-X(L)) more than 2-fold, showing a possible gene regulatory role of EGCG. The continual expression in p21WAF1 suggests that EGCG acts in the same way with p53 proteins to facilitate apoptosis after EGCG treatment. And Bax, PCNA, and Bcl-X are important in EGCG-mediated apoptosis. In contrast, CDK4 and Rb are not important in ovarian cancer cell growth inhibition.
  
  
  CONCLUSIONS
  EGCG can inhibit ovarian cancer cell growth through induction of apoptosis and cell cycle arrest as well as regulation of cell cycle-related proteins. Thereby, the EGCG-mediated apoptosis can be applied to an advanced strategy in the development of a potential drug against ovarian cancer.
authors.affiliation: Catholic Research Institutes of Medical Science, Seoul, South Korea.
authors.forename: Seung Won
authors.initials: SW
authors.lastname: Huh
authors.forename: Su Mi
authors.initials: SM
authors.lastname: Bae
authors.forename: Yong-Wan
authors.initials: YW
authors.lastname: Kim
authors.forename: Joon Mo
authors.initials: JM
authors.lastname: Lee
authors.forename: Sung Eun
authors.initials: SE
authors.lastname: Namkoong
authors.forename: Insu P
authors.initials: IP
authors.lastname: Lee
authors.forename: Sang Hee
authors.initials: SH
authors.lastname: Kim
authors.forename: Chong Kook
authors.initials: CK
authors.lastname: Kim
authors.forename: Woong Shick
authors.initials: WS
authors.lastname: Ahn
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000493:pharmacokinetics / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D002392:Catechin / Q000031:analogs & derivatives* / Q000493:pharmacokinetics / Q000494:pharmacology*; D064199:Cdc20 Proteins; D002453:Cell Cycle / Q000187:drug effects; D018797:Cell Cycle Proteins / Q000096:biosynthesis / Q000235:genetics; D002455:Cell Division / Q000187:drug effects; D045744:Cell Line, Tumor; D019925:Cyclin A / Q000096:biosynthesis / Q000235:genetics; D019926:Cyclin B / Q000096:biosynthesis / Q000235:genetics; D056744:Cyclin B1; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D010051:Ovarian Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics
chemical_list: D000972:Antineoplastic Agents, Phytogenic; C534699:CCNB1 protein, human; D064199:Cdc20 Proteins; D018797:Cell Cycle Proteins; D019925:Cyclin A; D019926:Cyclin B; D056744:Cyclin B1; D012333:RNA, Messenger; C577488:CDC20 protein, human; D002392:Catechin; C045651:epigallocatechin gallate