Skip Navigation


Carcinogenesis Advance Access originally published online on March 25, 2004
Carcinogenesis 2004 25(8):1359-1370; doi:10.1093/carcin/bgh144
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
25/8/1359    most recent
bgh144v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (29)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Trzeciak, A. R.
Right arrow Articles by Evans, M. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Trzeciak, A. R.
Right arrow Articles by Evans, M. K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis vol.25 no.8 © Oxford University Press 2004; all rights reserved.

ARTICLE

Cellular repair of oxidatively induced DNA base lesions is defective in prostate cancer cell lines, PC-3 and DU-145

Andrzej R. Trzeciak1, Simon G. Nyaga1, Pawel Jaruga2,3, Althaf Lohani1, Miral Dizdaroglu3 and Michele K. Evans1,4

1 Laboratory of Cellular and Molecular Biology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224-6825, 2 Department of Chemical and Biochemical Engineering, University of Maryland Baltimore County, Baltimore, MD 21250 and 3 Chemical Science and Technology Laboratory, National Institute of Standards and Technology, Gaithersburg, MD 20899, USA

4 To whom correspondence should be addressed Email: me42v{at}nih.gov

Mutagenic oxidative DNA base damage increases with age in prostatic tissue. Various factors may influence this increase including: increased production of reactive oxygen species, increased susceptibility to oxidative stress, alterations in detoxifying enzyme levels or defects in DNA repair. Using liquid chromatography/mass spectrometry and gas chromatography/mass spectrometry, we show increased levels of oxidative DNA base lesions, 8-hydroxyguanine (8-oxoG), 8-hydroxyadenine (8-oxoA) and 5-hydroxycytosine (5OHC) over the baseline in PC-3 and DU-145 prostate cancer cells following exposure to ionizing radiation and a repair period. Nuclear extracts from PC-3 and DU-145 prostate cancer cell lines are defective in the incision of 8-oxoG, 5OHC and thymine glycol (TG) relative to the non-malignant prostate cell line. Consistent with reduced expression of OGG1 2a, incision of 8-oxoG is reduced in PC-3 and DU-145 mitochondrial extracts. We also show a correlation between severely defective incision of TG and 5OHC and reduced levels of NTH1 in PC-3 mitochondria. The antioxidant enzymes, glutathione peroxidase (GPx), catalase and superoxide dismutases (SOD1, SOD2), have altered expression patterns in these cancer cell lines. Genetic analysis of the OGG1 gene reveals that both PC-3 and DU-145 cell lines harbor polymorphisms associated with a higher susceptibility to certain cancers. These data suggest that the malignant phenotype in PC-3 and DU-145 cell lines may be associated with defects in base excision repair and alterations in expression of antioxidant enzymes.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Mol Cancer ResHome page
S. M. K. Pulukuri, J. A. Knost, N. Estes, and J. S. Rao
Small Interfering RNA-Directed Knockdown of Uracil DNA Glycosylase Induces Apoptosis and Sensitizes Human Prostate Cancer Cells to Genotoxic Stress
Mol. Cancer Res., August 1, 2009; 7(8): 1285 - 1293.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
S. Maynard, S. H. Schurman, C. Harboe, N. C. de Souza-Pinto, and V. A. Bohr
Base excision repair of oxidative DNA damage and association with cancer and aging
Carcinogenesis, January 1, 2009; 30(1): 2 - 10.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Epidemiol. Biomarkers Prev.Home page
D. J. Waters, S. Shen, H. Xu, S. S. Kengeri, D. M. Cooley, E. C. Chiang, Y. Chen, D. Schlittler, C. Oteham, G. F. Combs Jr., et al.
Noninvasive Prediction of Prostatic DNA Damage by Oxidative Stress Challenge of Peripheral Blood Lymphocytes
Cancer Epidemiol. Biomarkers Prev., September 1, 2007; 16(9): 1906 - 1910.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Epidemiol. Biomarkers Prev.Home page
J.-Y. Choi, M. L. Neuhouser, M. Barnett, M. Hudson, A. R. Kristal, M. Thornquist, I. B. King, G. E. Goodman, and C. B. Ambrosone
Polymorphisms in Oxidative Stress-Related Genes Are Not Associated with Prostate Cancer Risk in Heavy Smokers
Cancer Epidemiol. Biomarkers Prev., June 1, 2007; 16(6): 1115 - 1120.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
P. Bonde, D. Gao, L. Chen, M. Duncan, T. Miyashita, E. Montgomery, J. W. Harmon, and C. Wei
Selective decrease in the DNA base excision repair pathway in squamous cell cancer of the esophagus
J. Thorac. Cardiovasc. Surg., January 1, 2007; 133(1): 74 - 81.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Epidemiol. Biomarkers Prev.Home page
B. A. Sokhansanj and D. M. Wilson III
Estimating the effect of human base excision repair protein variants on the repair of oxidative DNA base damage.
Cancer Epidemiol. Biomarkers Prev., May 1, 2006; 15(5): 1000 - 1008.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
J. W. Hill and M. K. Evans
Dimerization and opposite base-dependent catalytic impairment of polymorphic S326C OGG1 glycosylase
Nucleic Acids Res., March 20, 2006; 34(5): 1620 - 1632.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Cancer Res.Home page
C. J.M. Best, J. W. Gillespie, Y. Yi, G. V.R. Chandramouli, M. A. Perlmutter, Y. Gathright, H. S. Erickson, L. Georgevich, M. A. Tangrea, P. H. Duray, et al.
Molecular Alterations in Primary Prostate Cancer after Androgen Ablation Therapy
Clin. Cancer Res., October 1, 2005; 11(19): 6823 - 6834.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.