Sorbus rufopilosa Extract Exhibits Antioxidant and Anticancer Activities by Inducing Cell Cycle Arrest and Apoptosis in Human Colon Adenocarcinoma HT29 Cells.
10.15430/JCP.2016.21.4.249
- Author:
You Na OH
1
;
Soojung JIN
;
Hyun Jin PARK
;
Hyun Ju KWON
;
Byung Woo KIM
Author Information
1. Blue-Bio Industry Regional Innovation Center, Dong-Eui University, Busan, Korea. bwkim@deu.ac.kr
- Publication Type:Original Article
- Keywords:
Anticancer;
Antioxidant;
Apoptosis;
Cell cycle arrest;
Sorbus rufopilosa
- MeSH:
Adenocarcinoma*;
Apoptosis*;
Blotting, Western;
Caspase 3;
CDC2 Protein Kinase;
Cell Cycle Checkpoints*;
Cell Cycle*;
Colon*;
Cyclin B;
Ethanol;
Far East;
Flow Cytometry;
HT29 Cells*;
Humans*;
Rosacea;
Rosaceae;
Sorbus*;
Trees;
Up-Regulation
- From:Journal of Cancer Prevention
2016;21(4):249-256
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Sorbus rufopilosa, a tsema rowan, is a species of the small ornamental trees in the genus Sorbus and the family Rosaceae found in East Asia. The bioactivities of S. rufopilosa have not yet been fully determined. The objective of this study is to evaluate the antioxidant and anticancer effects of ethanol extract of S. rufopilosa (EESR) and to determine the molecular mechanism of its anticancer activity in human colon carcinoma HT29 cells. METHODS: To examine the antioxidant activity of EESR, 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity assay was performed. Inhibitory effect of EESR on cancer cell growth and proliferation was determined by water-soluble tetrazolium salt assay. To investigate the mechanism of EESR-mediated cytotoxicity, HT29 cells were treated with various concentrations of EESR and the induction of cell cycle arrest and apoptosis was analyzed by flow cytometry, 4,6-diamidino-2-phenylindole staining, and Western blot analysis. RESULTS: EESR showed significant antioxidant activity and inhibitory effect on HT29 cell growth in a dose-dependent manner. EESR induced cell cycle arrest at G2/M phase in a dose-dependent manner by modulating cyclin B, cyclin-dependent kinase 1 (CDK1), and CDK inhibitor p21 expression. EESR-induced apoptosis was associated with the upregulation of p53, a death receptor Fas, and a pro-apoptotic protein Bax and the activation of caspase 3, 8, and 9, resulting in the degradation of PARP. CONCLUSIONS: EESR possessing antioxidant activity efficiently inhibits proliferation of HT29 cells by inducing both cell cycle arrest and apoptosis. EESR may be a possible candidate for the anticancer drug development.
