Document Detail


Delta9-tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation.
MedLine Citation:
PMID:  16818634     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
It has been proposed that cannabinoids are involved in the control of cell fate. Thus, these compounds can modulate proliferation, differentiation, and survival in different manners depending on the cell type and its physiopathologic context. However, little is known about the effect of cannabinoids on the cell cycle, the main process controlling cell fate. Here, we show that Delta(9)-tetrahydrocannabinol (THC), through activation of CB(2) cannabinoid receptors, reduces human breast cancer cell proliferation by blocking the progression of the cell cycle and by inducing apoptosis. In particular, THC arrests cells in G(2)-M via down-regulation of Cdc2, as suggested by the decreased sensitivity to THC acquired by Cdc2-overexpressing cells. Of interest, the proliferation pattern of normal human mammary epithelial cells was much less affected by THC. We also analyzed by real-time quantitative PCR the expression of CB(1) and CB(2) cannabinoid receptors in a series of human breast tumor and nontumor samples. We found a correlation between CB(2) expression and histologic grade of the tumors. There was also an association between CB(2) expression and other markers of prognostic and predictive value, such as estrogen receptor, progesterone receptor, and ERBB2/HER-2 oncogene. Importantly, no significant CB(2) expression was detected in nontumor breast tissue. Taken together, these data might set the bases for a cannabinoid therapy for the management of breast cancer.
Authors:
María M Caffarel; David Sarrió; José Palacios; Manuel Guzmán; Cristina Sánchez
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cancer research     Volume:  66     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  2006 Jul 
Date Detail:
Created Date:  2006-07-04     Completed Date:  2006-09-07     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  6615-21     Citation Subset:  IM    
Affiliation:
Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects
Breast Neoplasms / drug therapy,  enzymology,  metabolism,  pathology*
CDC2 Protein Kinase / biosynthesis*,  genetics
Cell Cycle / drug effects*
Cell Division / drug effects
Cell Growth Processes / drug effects
Cell Line, Tumor
Down-Regulation / drug effects
G2 Phase / drug effects
Humans
RNA, Messenger / biosynthesis,  genetics
Receptor, Cannabinoid, CB1 / biosynthesis,  genetics
Receptor, Cannabinoid, CB2 / biosynthesis,  genetics
Tetrahydrocannabinol / pharmacology*
Chemical
Reg. No./Substance:
0/RNA, Messenger; 0/Receptor, Cannabinoid, CB1; 0/Receptor, Cannabinoid, CB2; 1972-08-3/Tetrahydrocannabinol; EC 2.7.11.22/CDC2 Protein Kinase

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