期刊
MOLECULAR CARCINOGENESIS
卷 45, 期 6, 页码 443-446出版社
WILEY
DOI: 10.1002/mc.20224
关键词
histone deacetylase; chromatin remodeling; sulforaphane; garlic; S-allyl compounds; butyrate; chemoprevention
资金
- NCI NIH HHS [CA90890, CA65525, P01 CA090890-01A29001, CA80176, R01 CA065525-08, R29 CA065525, P01 CA090890, R01 CA080176, P01 CA090890-01A20003, R01 CA080176-05, R01 CA065525-09, R01 CA065525, P01 CA090890-05] Funding Source: Medline
In cancer cells, an imbalance often exists between histone acetyltransferase (HAT) and histone deacetylase (HDAC) activities, and various drug companies are actively seeking competitive HDAC inhibitors for chemotherapeutic intervention. Cancer cells appear to be more sensitive than nontransformed cells to HDAC inhibitors, which disrupt the cell cycle and induce apoptosis via derepression of genes such as P21 and BAX However, in the search for potent HDAC inhibitors with cancer therapeutic potential, a tendency exists to overlook or dismiss weak ligands that could prove effective in cancer prevention. Butyrate, diallyl disulfide (DADS), and sulforaphane (SFN) are three dietary agents that exhibit HDAC inhibitory activity in vitro and/or in vivo, and other such dietary agents probably will be discovered that affect HDAC activity. We make the distinction between 'pharmacologic' agents that potently derepress gene expression, during therapeutic intervention, and dietary HDAC inhibitors that, as weak ligands, might subtly regulate the expression of genes involved in cell growth and apoptosis. An important issue for future study is to determine the extent to which dietary HDAC inhibitors, by modulating genes such as p21 and Bax, enable normal, nontransformed cells to respond most effectively to external stimuli and toxic insults. (c) 2006 Wiley-Liss, Inc.
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