Effects of ginsenoside Rh2(GS-Rh2) on cell cycle of Eca-109 esophageal carcinoma cell line.
- Author:
Li LI
1
;
Feng-ying QI
;
Jun-ru LIU
;
Lian-fu ZUO
Author Information
- Publication Type:Journal Article
- MeSH: Carcinoma, Squamous Cell; pathology; Cell Cycle; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Cyclin E; biosynthesis; genetics; Cyclin-Dependent Kinase 2; biosynthesis; genetics; Cyclin-Dependent Kinase Inhibitor p21; biosynthesis; genetics; Dose-Response Relationship, Drug; Drugs, Chinese Herbal; administration & dosage; isolation & purification; pharmacology; Esophageal Neoplasms; metabolism; pathology; Ginsenosides; administration & dosage; isolation & purification; pharmacology; Humans; Panax; chemistry; Plants, Medicinal; chemistry; RNA, Messenger; biosynthesis; genetics; Time Factors
- From: China Journal of Chinese Materia Medica 2005;30(20):1617-1621
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of ginsenoside Rh2 (GS-Rh2) on growth inhibition and cell cycle of Eca-109 esophageal carcinoma cell line in culture.
METHODThe 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.
RESULTGS-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.
CONCLUSIONGS-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.
