Document Detail

Cordycepin induces apoptosis by enhancing JNK and p38 kinase activity and increasing the protein expression of Bcl-2 pro-apoptotic molecules.
MedLine Citation:
PMID:  20803769     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: To explore the molecular mechanism by which cordycepin inhibits cell proliferation and induces apoptosis of human colorectal cancer cells.
METHODS: Cell counting and MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfopheny)-2H-tetrazolium, inner salt) method were used to monitor the effects of cordycepin on cell proliferation. Flow cytometry (FCM) was used to analyze the effects of cordycepin on the cell cycle progress. Annexin V-fluorescein isothiocyanate (FITC) analysis was used to detect apoptosis at a very early stage. Caspase-Glo was used to determine caspase activity and Western blot was used to measure protein expression levels of c-Jun N-terminal kinase (JNK), p38, and Bcl-2 pro-apoptosis family.
RESULTS: The numbers of viable SW480 and SW620 cells and the proliferation of these cells were significantly reduced with increases in cordycepin concentration (P<0.01). The cell cycle progression of SW480 and SW620 was arrested at the G0/G1 phase by the addition of cordycepin, and apoptosis rates of cordycepin treatments were increased compared with the control group. Cordycepin-treated cells showed phosphatidylserine valgus, suggesting the existence of early apoptosis. Caspase-3/7 and -9 activity significantly increased and the protein expression levels of JNK, p38, and Bax, Bid, Bim, and Puma from Bcl-2 pro-apoptosis molecules also increased after the treatment with cordycepin.
CONCLUSIONS: Cordycepin can inhibit SW480 and SW620 cell proliferation and induce apoptosis. Apoptosis might be induced by enhancing JNK and p38 kinase activity and increasing the protein expression of Bcl-2 pro-apoptotic molecules.
Wei He; Mei-fang Zhang; Jun Ye; Ting-ting Jiang; Xu Fang; Ying Song
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of Zhejiang University. Science. B     Volume:  11     ISSN:  1862-1783     ISO Abbreviation:  J Zhejiang Univ Sci B     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-30     Completed Date:  2011-01-04     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  101236535     Medline TA:  J Zhejiang Univ Sci B     Country:  China    
Other Details:
Languages:  eng     Pagination:  654-60     Citation Subset:  IM    
The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
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MeSH Terms
Antineoplastic Agents / pharmacology*,  therapeutic use*
Apoptosis / drug effects,  immunology*
Blotting, Western
Cell Cycle / immunology
Cell Line, Tumor
Cell Proliferation
Colorectal Neoplasms / drug therapy*,  enzymology,  immunology
Deoxyadenosines / pharmacology*,  therapeutic use
Dose-Response Relationship, Drug
Flow Cytometry
JNK Mitogen-Activated Protein Kinases / immunology
Proto-Oncogene Proteins c-bcl-2 / metabolism
p38 Mitogen-Activated Protein Kinases / immunology
Reg. No./Substance:
0/Antineoplastic Agents; 0/Deoxyadenosines; 0/Proto-Oncogene Proteins c-bcl-2; 73-03-0/cordycepin; EC Mitogen-Activated Protein Kinases; EC Mitogen-Activated Protein Kinases

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