NDLI: A novel prodrug of epigallocatechin-3-gallate: differential epigenetic hTERT repression in human breast cancer cells.

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A novel prodrug of epigallocatechin-3-gallate: differential epigenetic hTERT repression in human breast cancer cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Meeran, Syed M. Patel, Shweta N. Chan, Tak-Hang Tollefsbol, Trygve O.
Description	Country affiliation: United States Author Affiliation: Meeran SM ( Department of Biology, University of Alabama at Birmingham, 1300 University Boulevard, Campbell Hall 175, Birmingham, AL 35294-1170, USA. musthapa@uab.edu)
Abstract	Epigallocatechin-3-gallate (EGCG), a major component of green tea polyphenols (GTP), has been reported to downregulate telomerase activity in breast cancer cells thereby increasing cellular apoptosis and inhibiting cellular proliferation. However, the major concerns with GTPs are their bioavailability and stability under physiologic conditions. In the present study, we show that treatments with EGCG and a novel prodrug of EGCG (pro-EGCG or pEGCG) dose- and time-dependently inhibited the proliferation of human breast cancer MCF-7 and MDA-MB-231 cells but not normal control MCF10A cells. Furthermore, both EGCG and pro-EGCG inhibited the transcription of hTERT (human telomerase reverse transcriptase), the catalytic subunit of telomerase, through epigenetic mechanisms in estrogen receptor (ER)-positive MCF-7 and ER-negative MDA-MB-231 cells. The downregulation of hTERT expression was found to be because of hTERT promoter hypomethylation and histone deacetylations, mediated at least partially through inhibition of DNA methyltransferase and histone acetyltransferase activities, respectively. In addition, we also observed that EGCG and pEGCG can remodel chromatin structures of the hTERT promoter by decreasing the level of acetyl-H3, acetyl-H3K9, and acetyl-H4 to the hTERT promoter. EGCG and pEGCG induced chromatin alterations that facilitated the binding of many hTERT repressors such as MAD1 and E2F-1 to the hTERT regulatory region. Depletion of E2F-1 and MAD1 by using siRNA reversed the pEGCG downregulated hTERT expression and associated cellular apoptosis differently in ER-positive and ER-negative breast cancer cells. Collectively, our data provide new insights into breast cancer prevention through epigenetic modulation of telomerase by using pro-EGCG, a more stable form of EGCG, as a novel chemopreventive compound.
File Format	HTM / HTML
ISSN	19406207
e-ISSN	19406215
DOI	10.1158/1940-6207.CAPR-11-0009
Journal	Cancer Prevention Research
Issue Number	8
Volume Number	4
Language	English
Publisher	American Association for Cancer Research
Publisher Date	2011-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Oncology Anticarcinogenic Agents Pharmacology Breast Neoplasms Genetics Catechin Analogs & Derivatives Epigenesis, Genetic Prodrugs Telomerase Chemistry Apoptosis Cell Line, Tumor Cell Proliferation Dna Modification Methylases Metabolism Flow Cytometry Histone Acetyltransferases Promoter Regions, Genetic Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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