Document Detail


DNA repair is indispensable for survival after acute inflammation.
MedLine Citation:
PMID:  22684101     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
More than 15% of cancer deaths worldwide are associated with underlying infections or inflammatory conditions, therefore understanding how inflammation contributes to cancer etiology is important for both cancer prevention and treatment. Inflamed tissues are known to harbor elevated etheno-base (ε-base) DNA lesions induced by the lipid peroxidation that is stimulated by reactive oxygen and nitrogen species (RONS) released from activated neutrophils and macrophages. Inflammation contributes to carcinogenesis in part via RONS-induced cytotoxic and mutagenic DNA lesions, including ε-base lesions. The mouse alkyl adenine DNA glycosylase (AAG, also known as MPG) recognizes such base lesions, thus protecting against inflammation-associated colon cancer. Two other DNA repair enzymes are known to repair ε-base lesions, namely ALKBH2 and ALKBH3; thus, we sought to determine whether these DNA dioxygenase enzymes could protect against chronic inflammation-mediated colon carcinogenesis. Using established chemically induced colitis and colon cancer models in mice, we show here that ALKBH2 and ALKBH3 provide cancer protection similar to that of the DNA glycosylase AAG. Moreover, Alkbh2 and Alkbh3 each display apparent epistasis with Aag. Surprisingly, deficiency in all 3 DNA repair enzymes confers a massively synergistic phenotype, such that animals lacking all 3 DNA repair enzymes cannot survive even a single bout of chemically induced colitis.
Authors:
Jennifer A Calvo; Lisiane B Meira; Chun-Yue I Lee; Catherine A Moroski-Erkul; Nona Abolhassani; Koli Taghizadeh; Lindsey W Eichinger; Sureshkumar Muthupalani; Line M Nordstrand; Arne Klungland; Leona D Samson
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-06-11
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  122     ISSN:  1558-8238     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-07-03     Completed Date:  2012-09-11     Revised Date:  2013-05-20    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2680-9     Citation Subset:  AIM; IM    
Affiliation:
Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Azoxymethane / pharmacology
Carcinogens / pharmacology
Colitis / chemically induced,  genetics*,  metabolism
Colon / immunology,  pathology
Colorectal Neoplasms / chemically induced,  genetics,  metabolism
DNA Glycosylases / genetics*,  metabolism
DNA Repair*
DNA Repair Enzymes / genetics*,  metabolism
Dextran Sulfate / pharmacology
Dioxygenases / genetics*,  metabolism
Epistasis, Genetic
Female
Genetic Predisposition to Disease
Kaplan-Meier Estimate
Lethal Dose 50
Lipopolysaccharides / pharmacology
Male
Mice
Mice, 129 Strain
Mice, Inbred C57BL
Mice, Knockout
Pancreas / immunology,  pathology
Pancreatitis / chemically induced,  genetics*,  metabolism
Grant Support
ID/Acronym/Agency:
P30 ES002109/ES/NIEHS NIH HHS; P30-ES02109/ES/NIEHS NIH HHS; R01 CA055042/CA/NCI NIH HHS; R01 CA075576/CA/NCI NIH HHS; R01 CA149261/CA/NCI NIH HHS; R01-CA055042/CA/NCI NIH HHS; R01-CA075576/CA/NCI NIH HHS; R01-CA149261/CA/NCI NIH HHS; T32-ES007020/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Carcinogens; 0/Lipopolysaccharides; 25843-45-2/Azoxymethane; 9042-14-2/Dextran Sulfate; EC 1.13.11.-/Dioxygenases; EC 1.14.11.-/ABH3 protein, mouse; EC 1.14.11.-/Alkbh2 protein, mouse; EC 3.2.2.-/3-methyladenine-DNA glycosylase; EC 3.2.2.-/DNA Glycosylases; EC 6.5.1.-/DNA Repair Enzymes
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Ynamides: stable ligand equivalents of unstable oxazol-4-ylidenes (novel mesoionic carbenes).
Next Document:  Periostin promotes chronic allergic inflammation in response to Th2 cytokines.