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PMID: 15251435 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Histone deacetylase inhibitors regulate p21WAF1 gene expression at the post-transcriptional level in HepG2 cells.

FEBS letters ·Vol. 570 ·No. 1-3 ·2004-07-16 ·Pages 37-40

Hirsch CL, Bonham K

Abstract

Histone deacetylase inhibitors (HDIs) are thought to act primarily at the level of transcription inducing cell cycle arrest, differentiation and/or apoptosis in many cancer cell types. Induction of the potent cdk/cyclin inhibitor p21WAF1 is a key feature of this HDI mediated transcriptional re-programming phenomenon. However, in the current study we report that HDIs are also capable of inducing p21WAF1 through purely post-transcriptional events, namely increased mRNA stability. These studies highlight our growing appreciation for the complexities of HDI mediated effects and challenge our preconceptions regarding the action of these promising anti-neoplastics.

MeSH Terms
Apoptosis Blotting, Northern Cell Differentiation Cell Division Cell Line Chloramphenicol O-Acetyltransferase/metabolism Cyclin-Dependent Kinase Inhibitor p21 Cyclins/metabolism Dose-Response Relationship, Drug Enzyme Inhibitors/pharmacology Gene Expression Regulation Histone Deacetylase Inhibitors Histones/metabolism Humans Immunoblotting Luciferases/metabolism Plasmids/metabolism Promoter Regions, Genetic RNA/metabolism RNA, Messenger/metabolism Time Factors Transcription, Genetic Transcriptional Activation Transfection
Chemicals
CDKN1A protein, human Cyclin-Dependent Kinase Inhibitor p21 Cyclins Enzyme Inhibitors Histone Deacetylase Inhibitors Histones RNA, Messenger RNA Luciferases Chloramphenicol O-Acetyltransferase
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Hirsch Calley L
Department of Biochemistry, University of Saskatchewan, Saskatoon SK, Canada S7N 5E5.
Bonham Keith
Article Info
Journal
FEBS letters
Abbr.
FEBS Lett
ISSN
0014-5793
Published
2004-07-16
Pages
37-40
Language
English
Region
England
NLM ID
0155157
Subset
IM
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