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Specific and redundant functions of histone deacetylases in regulation of cell cycle and apoptosis.
Cell Cycle 3, 115-117 (2004)
Inappropriate control of expression of genetic information is the cause of many forms ofcancer. Aberrant transcriptional repression by recruitment of histone deacetylases (HDACs) isa key step in pathogenesis of myeloid leukemia. We recently reported that development ofcolonic cancer involves alterations in the transcriptional repression machinery by increasedexpression of HDAC 2 upon loss of the APC tumor suppressor. Increased expression ofHDAC 2 is essential for prevention of apoptosis of HT-29 colonic cancer cells. We nowdiscuss whether HDAC 2 also plays a role for aberrant cell cycle regulation and expression ofthe p21Cip/Waf cell cycle inhibitor. Whereas inhibition of HDACs by valproic acid ortrichostatin A increases p21 expression, selective interference with HDAC 2 by siRNAtransfection or reconstitution of wildtype APC does not affect p21 expression. Likewise,treatment of HT-29 cells with the HDAC inhibitor valproic acid leads to a moderate inhibitionof cell cycle progression in the G1 phase whereas interference with HDAC2 expression doesnot. Thus, HDAC 2 appears to serve a preferential role in the prevention of apoptosis and notin cell cycle control similar to the specific importance of HDAC 1 for cell cycle regulation orHDAC 9 for the stress response of the heart.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
cell cycle; apoptosis; cancer treatment; histone deacetylases; HDAC inhibitors; colon cancer; myeloid leukemia
Language
english
Publication Year
2004
HGF-reported in Year
0
ISSN (print) / ISBN
1538-4101
e-ISSN
1551-4005
Journal
Cell Cycle
Quellenangaben
Volume: 3,
Issue: 10,
Pages: 115-117
Publisher
Landes Bioscience
Reviewing status
Peer reviewed
POF-Topic(s)
30203 - Molecular Targets and Therapies
Research field(s)
Enabling and Novel Technologies
PSP Element(s)
G-505200-001
Erfassungsdatum
2004-10-29