Journal
CARCINOGENESIS
Volume 30, Issue 10, Pages 1776-1780Publisher
OXFORD UNIV PRESS
DOI: 10.1093/carcin/bgp146
Keywords
-
Categories
Funding
- US Department of Defense Prostate Cancer Research Program [DAMD17-02-1-0052]
- US Department of Energy Low Dose Research Program [DE-FG02-03ER63635]
- National Aeronautics and Space Administration [NAG2-1629]
Ask authors/readers for more resources
Caspase-activated DNase (CAD), also called DNA fragmentation factor (DFF), is the enzyme responsible for DNA fragmentation during apoptosis, a hallmark of programmed cell death. CAD/DFF has been shown to suppress radiation-induced carcinogenesis by preventing genomic instability in cells. In this study, we have investigated the role of CAD in chemical carcinogenesis using CAD-null mice and two-stage model of skin carcinogenesis. After topical treatment of mouse skin with dimethylbenz[a]anthracene (DMBA) as an initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as a promoting agent, there was a 4-fold increase in the number of papillomas per mouse and 50.8% increase in the incidence of papilloma formation in the CAD knockout mice compared with wild-type littermates. The papillomas in CAD-null mice grew faster and reached larger sizes. These data indicate that loss of CAD function enhances tumorigenesis induced by a chemical carcinogen in the DMBA/TPA two-stage model of skin carcinogenesis in mice.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available