title: [Effects of ginsenoside Rh2(GS-Rh2) on cell cycle of Eca-109 esophageal carcinoma cell line].
abstract: OBJECTIVE
  To investigate the effects of ginsenoside Rh2 (GS-Rh2) on growth inhibition and cell cycle of Eca-109 esophageal carcinoma cell line in culture.
  
  
  METHODS
  The effects of GS-Rh2 on cell growth inhibition was detected by MTT assay. Cell cycle was analyzed by flow cytometry (FCM). Cell morphology was observed by a light microscope after HE staining. The protein expression of cell cycle components (cyclinE, CDK2, p21WAF1) were examined by immunocytochemistry and Western blot. The mRNA expression were examined by semiquantitative RT-PCR.
  
  
  RESULTS
  GS-Rh2 inhibited the proliferation of Eca-109 cells in dose and time-dependent manners. The inhibition rate was about 50% after 1-day treatment with 20 microg x mL(-1) GS-Rh2 x 20 microg x mL(-1) GS-Rh2 induced the mature differentiation and morphological reversion. With increasing dose of GS-Rh2 treatment, the cell number of G0/G1 phase was increased, whereas it decreased at S and G2/M phase. There was significant difference between 10, 20 microg x mL(-1) GS-Rh2 groups and the corresponding group without GS-Rh2 treatement. After treating cells by 20 microg x mL(-1) GS-Rh2 for 1, 2, 3 days individually, the protein and mRNA expression of both cyclinE and CDK2 reduced, while the expression of p21WAF1 enhanced gradually.
  
  
  CONCLUSIONS
  GS-Rh2 could arrest Eca-109 cells at G0/G1 phase and induce cell differentiation tending to normal. Furthermore, GS-Rh2 had an effect on expression of cell cycle components (cyclinE, CDK2 and p21WAF1) to inhibit Eca-109 cell proliferation.
authors.affiliation: Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Feng-ying
authors.initials: FY
authors.lastname: Qi
authors.forename: Jun-ru
authors.initials: JR
authors.lastname: Liu
authors.forename: Lian-fu
authors.initials: LF
authors.lastname: Zuo
mesh_terms: D002294:Carcinoma, Squamous Cell / Q000473:pathology; D002453:Cell Cycle / Q000187:drug effects*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D019927:Cyclin E / Q000096:biosynthesis / Q000235:genetics; D051357:Cyclin-Dependent Kinase 2 / Q000096:biosynthesis / Q000235:genetics; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000096:biosynthesis / Q000235:genetics; D004305:Dose-Response Relationship, Drug; D004365:Drugs, Chinese Herbal / Q000008:administration & dosage / Q000302:isolation & purification / Q000494:pharmacology*; D004938:Esophageal Neoplasms / Q000378:metabolism / Q000473:pathology*; D036145:Ginsenosides / Q000008:administration & dosage / Q000302:isolation & purification / Q000494:pharmacology*; D006801:Humans; D005894:Panax / Q000737:chemistry; D010946:Plants, Medicinal / Q000737:chemistry; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D013997:Time Factors
chemical_list: C493956:CDKN1A protein, human; D019927:Cyclin E; D050759:Cyclin-Dependent Kinase Inhibitor p21; D004365:Drugs, Chinese Herbal; D036145:Ginsenosides; D012333:RNA, Messenger; C055305:ginsenoside Rh2; C495894:CDK2 protein, human; D051357:Cyclin-Dependent Kinase 2