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Xanthorrhizol, a natural sesquiterpenoid, induces apoptosis and growth arrest in HCT116 human colon cancer cells.

Authors
 You-Jin Kang  ;  Kwang-Kyun Park  ;  Won-Yoon Chung  ;  Jae-Kwan Hwang  ;  Sang Kook Lee 
Citation
 JOURNAL OF PHARMACOLOGICAL SCIENCES, Vol.111(3) : 276-284, 2009 
Journal Title
 JOURNAL OF PHARMACOLOGICAL SCIENCES 
ISSN
 1347-8613 
Issue Date
2009
MeSH
Antineoplastic Agents, Phytogenic* ; Apoptosis/drug effects* ; Apoptosis Regulatory Proteins/biosynthesis ; Apoptosis Regulatory Proteins/genetics ; Blotting, Western ; Cell Cycle/drug effects ; Cell Cycle Proteins/biosynthesis ; Cell Cycle Proteins/genetics ; Cell Division/drug effects ; Cell Proliferation/drug effects ; Cyclin-Dependent Kinases/metabolism ; DNA Fragmentation ; Flow Cytometry ; Genes, Reporter ; Growth Differentiation Factor 15/metabolism ; HCT116 Cells ; Humans ; Indicators and Reagents ; Phenols/pharmacology*
Keywords
apoptosis ; cell cycle arrest ; HCT116 human colon cancer cell ; non-steroidal anti-inflammatory drug–activated gene-1 (NAG-1) expression ; xanthorrhizol
Abstract
Xanthorrhizol is a sesquiterpenoid from the rhizome of Curcuma xanthorrhiza. In our previous studies, xanthorrhizol suppressed cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression, inhibited cancer cell growth, and exerted an anti-metastatic effect in an animal model. However, the exact mechanisms for its inhibitory effects against cancer cell growth have not yet been fully elucidated. In the present study, we investigated the growth inhibitory effect of xanthorrhizol on cancer cells. Xanthorrhizol dose-dependently exerted antiproliferative effects against HCT116 human colon cancer cells. Xanthorrhizol also arrested cell cycle progression in the G0/G1 and G2/M phase and induced the increase of sub-G1 peaks. Cell cycle arrest was highly correlated with the downregulation of cyclin A, cyclin B1, and cyclin D1; cyclin-dependent kinase 1 (CDK1), CDK2, and CDK4; proliferating cell nuclear antigen; and inductions of p21 and p27, cyclin-dependent kinase inhibitors. The apoptosis by xanthorrhizol was markedly evidenced by induction of DNA fragmentation, release of cytochrome c, activation of caspases, and cleavage of poly-(ADP-ribose) polymerase. In addition, xanthorrhizol increased the expression and promoter activity of pro-apoptotic non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1). These findings provide one plausible mechanism for the growth inhibitory activity of xanthorrhizol against cancer cells.
Files in This Item:
T200903870.pdf Download
DOI
10.1254/jphs.09141FP
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
Yonsei Authors
Park, Kwang Kyun(박광균)
Chung, Won Yoon(정원윤) ORCID logo https://orcid.org/0000-0001-8428-9005
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/105410
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