期刊
FOOD AND CHEMICAL TOXICOLOGY
卷 48, 期 1, 页码 277-283出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2009.09.042
关键词
Cordycepin; Colon cancer cells; JNK1; G2/M-phase cell-cycle arrest; p21WAF1; Cell growth inhibition
资金
- Korean government (MEST) [R11-2008-014-01001]
Cordycepin (3'-deoxyadenosine) has many anti-cancer properties. However, neither its molecular mechanism nor its molecular targets are well understood. In the present study, we investigated novel molecular mechanisms for the anti-tumor effects of cordycepin in human colon cancer HCT116 cells. After treatment of cells with cordycepin, dose-dependent cell growth inhibition was observed at an IC50 value of 200 mu M. Cordycepin treatment resulted in G2/M-phase cell-cycle arrest, which was associated with increased p21WAF1 levels and reduced amounts of cyclin B1, Cdc2, and Cdc25c in a p53-independent pathway. Moreover, cordycepin treatment induced activation of JNK (c-Jun N-terminal kinases). Pretreatment with SP600125, a JNK-specific inhibitor, abrogated cordycepin-mediated p21WAF1 expression, cell growth inhibition, and reduced cell-cycle proteins. Furthermore, JNK1 inhibition by small interfering RNA (siRNA) produced similar results: suppression of cordycepin-induced p21WAF1 expression. decreased cell growth, and reduced cell-cycle proteins. Together, these results suggest a critical role for JNK1 activation in cordycepin-induced inhibition of cell growth and G2/M-phase arrest in human colon cancer cells. (c) 2009 Elsevier Ltd. All rights reserved.
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