Histone deacetylase inhibitors as potential anti-skin cancer agents

Saunders, N, Dicker, A. J., Popa, C., Jones, S. J. and Dahler, A. L. (1999) Histone deacetylase inhibitors as potential anti-skin cancer agents. Cancer Research, 59 2: 399-404.


Author Saunders, N
Dicker, A. J.
Popa, C.
Jones, S. J.
Dahler, A. L.
Title Histone deacetylase inhibitors as potential anti-skin cancer agents
Journal name Cancer Research   Check publisher's open access policy
ISSN 0008-5472
Publication date 1999-01-01
Year available 1999
Sub-type Article (original research)
Open Access Status Not yet assessed
Volume 59
Issue 2
Start page 399
End page 404
Total pages 6
Place of publication New Jersey, USA
Publisher American Association for Cancer Res.
Language eng
Subject C1
321015 Oncology and Carcinogenesis
730108 Cancer and related disorders
Abstract The regulation of squamous differentiation is a tightly regulated process involving transcriptional repression and activation. Previous studies have established that squamous carcinoma cell lines inappropriately regulate the transcription of genes important to the control of squamous differentiation. Histone deactylase inhibitors such as trichostatin A (TSA) and butyrate disrupt normal chromatin structure and cause alterations in gene expression/regulation. For these reasons, we examined the effects of both butyrate and TSA on the growth and differentiation of human keratinocytes or squamous carcinoma cells in tissue culture. We found that treatment of keratinocytes or squamous carcinoma cells with butyrate induced a reversible growth arrest. TSA, on the other hand, induced an irreversible growth arrest in both keratinocytes and squamous carcinoma cells. The growth arrest of keratinocytes induced by TSA or butyrate was accompanied by a reduction in the mRNA levels for proliferation gene cdk1 and an induction of the mRNA for the differentiation-specific transglutaminase type I gene (TG1). In contrast, the squamous carcinoma cells had decreased cdk1 and TG1 mRNA in response to TSA or butyrate, Both of these agents produced transient increases in the acetylation of histone H4 in keratinocytes and squamous carcinoma cells. These data indicated that TSA may have potential as a topical treatment for epidermal malignancies.
Keyword Oncology
Differentiation-specific Genes
Human Epidermal-keratinocytes
Cell-cycle Progression
Transcriptional Repression
Epithelial-cells
Interferon-gamma
Sodium-butyrate
Nucleosomal Dna
Trichostatin-a
Retinoic Acid
Q-Index Code C1
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: School of Medicine Publications
UQ Diamantina Institute Publications
 
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Created: Wed, 11 Jun 2008, 01:28:28 EST