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Carcinogenesis Advance Access first published online on November 4, 2004
This version published online on November 5, 2004
Carcinogenesis, doi:10.1093/carcin/bgh307
© 2004 by Oxford University Press
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Received June 29, 2004
Revised September 30, 2004
Accepted October 1, 2004

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

DNMT3B polymorphisms and risk of primary lung cancer

Su Jeong Lee 1, Hyo-Sung Jeon 1, Jin-Sung Jang 2, Sun Ha Park 1, Ga Young Lee 1, Byung-Heon Lee 2, Chang Ho Kim 3, Young Mo Kang 3, Won Kee Lee 4, Sin Kam 5, Rang Woon Park 2, In-San Kim 2, Young Lae Cho 6, Tae Hoon Jung 3, and Jae Yong Park 7*

1 Cancer Research Institute, Kyungpook National University Hospital, Samduk 2Ga 50, Daegu, 700-412, Korea
2 Department of Biochemistry, School of Medicine, Kyungpook National University, Dong In 2Ga 101, Daegu, 700-422, Korea
3 Department of Internal Medicine, School of Medicine, Kyungpook National University, Dong In 2Ga 101, Daegu, 700-422, Korea
4 Health Promotion Research Center, Kyungpook National University, Dong In 2Ga 101, Daegu, 700-422, Korea
5 Health Promotion Research Center, Kyungpook National University, Dong In 2Ga 101, Daegu, 700-422, Korea; Department of Preventive Medicine, School of Medicine, Kyungpook National University, Dong In 2Ga 101, Daegu, 700-422, Korea
6 Department of Obstetrics and Gynecology, School of Medicine, Kyungpook National University, Dong In 2Ga 101, Daegu, 700-422, Korea
7 Cancer Research Institute, Kyungpook National University Hospital, Samduk 2Ga 50, Daegu, 700-412, Korea; Department of Biochemistry, School of Medicine, Kyungpook National University, Dong In 2Ga 101, Daegu, 700-422, Korea; Department of Internal Medicine, School of Medicine, Kyungpook National University, Dong In 2Ga 101, Daegu, 700-422, Korea

* To whom correspondence should be addressed.
Jae Yong Park, E-mail: jaeyong{at}kyungpook.ac.kr


  Abstract

DNA-methyltransferase-3B (DNMT3B) plays an important role in the generation of aberrant methylation in carcinogenesis. Polymorphisms and haplotypes of DNMT3B gene may influence DNMT3B activity on DNA methylation, thereby modulating the susceptibility to lung cancer. To test this hypothesis, we investigated the association of the -283T>C (from exon 1A transcription start site) and -579G>T (from exon 1B transcription start site) polymorphisms in DNMT3B promoter, and their haplotypes with the risk of lung cancer in a Korean population. DNMT3B genotype was determined in 432 lung cancer patients and 432 healthy controls that were frequency-matched for age and sex. Individuals with at least one -283T allele were at a significantly decreased risk of adenocarcinoma (AC) and small cell carcinoma (SM) (adjusted OR = 0.48, 95% CI = 0.28-0.82, P = 0.007; and adjusted OR = 0.47, 95% CI = 0.24-0.93, P = 0.03, respectively) compared with those harboring -283CC genotype. Individuals with at least one -579G allele were also at a significantly decreased risk of AC and SM (adjusted OR = 0.47, 95% CI = 0.28-0.81, P = 0.006; and adjusted OR = 0.51, 95% CI = 0.26-0.99, P = 0.048, respectively) compared with those having -579TT genotype. The -283T allele was linked with -579G allele, and haplotype -283T/-579G was associated with a significantly decreased risk of AC (adjusted OR = 0.48, 95% CI = 0.29-0.81, P = 0.006) as compared with haplotype -283C/-579T. In a promoter assay, carriage of the -283T allele showed a significantly lower promoter activity (approximately 50%) compared with the -283C allele (P < 0.001), but the -579G>T polymorphism did not effect on the DNMT3B promoter activity. These results suggest that the DNMT3B -283T>C polymorphism influence DNMT3B expression, thus contributing to the genetic susceptibility to lung cancer.


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