Document Detail


Green tea polyphenol epigallocatechin inhibits DNA replication and consequently induces leukemia cell apoptosis.
MedLine Citation:
PMID:  11351279     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Consistent with the putative role of green tea in cancer prevention, tea polyphenols have previously been shown to inhibit tumor cell proliferation by inducing G1 or G2/M cell cycle arrests, also documented is their ability to induce apoptosis (programmed cell death). However, it is unclear whether or not the cell cycle effects of polyphenols are related to their cell death-inducing ability. Here we report that the tea polyphenol (-)-epigallocatechin (EGC) inhibits DNA replication in three leukemia cancer cell lines, Jurkat T, HL-60 and K562. Among all the tested tea polyphenols, EGC was found to be the most potent in accumulation of S phase cells and inhibition of the S-G2 progression. In addition, EGC-mediated inhibition of S phase progression results in induction of apoptosis, as determined by sub-G1 cell population, breakage of endonuclear DNA, cleavage of poly(ADP-ribose) polymerase and loss of cell viability. When used in cells containing low S and high G1 and G2/M populations, EGC did not induce apoptosis. Furthermore, EGC did not inhibit M-G1 transition. Our finding that EGC inhibits S phase progression that results in leukemia cell death provides a novel and plausible molecular mechanism for how green tea may inhibit the growth of rapidly proliferating neoplastic cells.
Authors:
D M Smith; Q P Dou
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  International journal of molecular medicine     Volume:  7     ISSN:  1107-3756     ISO Abbreviation:  Int. J. Mol. Med.     Publication Date:  2001 Jun 
Date Detail:
Created Date:  2001-05-14     Completed Date:  2001-07-19     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9810955     Medline TA:  Int J Mol Med     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  645-52     Citation Subset:  IM    
Affiliation:
Drug Discovery Program, H. Lee Moffitt Cancer Center and Research Institute, Interdisciplinary Oncology Program and Department of Biochemistry and Molecular Biology, College of Medicine, University of South Florida, Tampa, FL 33612, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis*
Catechin / analogs & derivatives,  pharmacology*
Cell Cycle / drug effects
Cell Division / drug effects
DNA / biosynthesis*,  drug effects
Dose-Response Relationship, Drug
Flavonoids*
Flow Cytometry
HL-60 Cells
Humans
In Situ Nick-End Labeling
Jurkat Cells
K562 Cells
Leukemia / pathology*
Models, Chemical
Phenols / pharmacology*
Plant Extracts / pharmacology*
Polymers / pharmacology*
Tea / chemistry*
Thymidine / metabolism
Time Factors
Grant Support
ID/Acronym/Agency:
AG13300/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/Flavonoids; 0/Phenols; 0/Plant Extracts; 0/Polymers; 0/Tea; 154-23-4/Catechin; 1617-55-6/gallocatechol; 50-89-5/Thymidine; 9007-49-2/DNA

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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