Arylamine N-acetyltransferase 1: A novel drug target in cancer development

Butcher, Neville J. and Minchin, Rodney F. (2012) Arylamine N-acetyltransferase 1: A novel drug target in cancer development. Pharmacological Reviews, 64 1: 147-165.


Author Butcher, Neville J.
Minchin, Rodney F.
Title Arylamine N-acetyltransferase 1: A novel drug target in cancer development
Formatted title Arylamine N-acetyltransferase 1: A novel drug target in cancer development
Journal name Pharmacological Reviews   Check publisher's open access policy
ISSN 0031-6997
1521-0081
Publication date 2012-01
Year available 2011
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1124/pr.110.004275
Volume 64
Issue 1
Start page 147
End page 165
Total pages 19
Place of publication Bethesda, MD, United States
Publisher American Society for Pharmacology and Experimental Therapeutics
Collection year 2012
Language eng
Formatted abstract The human arylamine N-acetyltransferases first attracted attention because of their role in drug metabolism. However, much of the current literature has focused on their role in the activation and detoxification of environmental carcinogens and how genetic polymorphisms in the genes create predispositions to increased or decreased cancer risk. There are two closely related genes on chromosome 8 that encode the two human arylamine N-acetyltransferases—NAT1 and NAT2. Although NAT2 has restricted tissue expression, NAT1 is found in almost all tissues of the body. There are several single-nucleotide polymorphisms in the protein coding and 3′-untranslated regions of the gene that affect enzyme activity. However, NAT1 is also regulated by post-translational and environmental factors, which may be of greater importance than genotype in determining tissue NAT1 activities. Recent studies have suggested a novel role for this enzyme in cancer cell growth. NAT1 is up-regulated in several cancer types, and overexpression can lead to increased survival and resistance to chemotherapy. Although a link to folate homeostasis has been suggested, many of the effects attributed to NAT1 and cancer cell growth remain to be explained. Nevertheless, the enzyme has emerged as a viable candidate for drug development, which should lead to small molecule inhibitors for preclinical and clinical evaluation.
Q-Index Code CX
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Published online before print November 16, 2011

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Non HERDC
School of Biomedical Sciences Publications
 
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