DNMT3b -149C/T promoter variants and methylation of colorectal cancer-associated genes

Cancer Biomark. 2015;15(3):227-33. doi: 10.3233/CBM-150463.

Abstract

Objective: DNMT3B overexpression has been linked with the CpG island methylator phenotype in various cancers. Considering the role of the DNMT3b -149C/T promoter polymorphism on the gene expression, we evaluated the associations of this polymorphism with colorectal cancer (CRC) risk and hypermethylation of six tumor suppressor genes in CRC tumors.

Methods: The DNMT3b was genotyped by PCR-RFLP in 108 sporadic CRC patients and 185 healthy controls and methylation of genes' promoter was determined by methylation specific PCR.

Results: In comparison to controls, the TT genotype was strongly associated with a high risk of cancer incidence (OR = 3.3, 95% CI = 1.6-6.9). The frequency of methylated hMLH1 was significantly higher in patients with the DNMT3bCT genotype (p= 0.03), especially in male subjects. The frequency of hMLH1 methylation was significantly higher in young patients (< 60 years) with the CT/TT genotypes. The combined CT/TT genotypes also showed significant associations with the ECAD methylation in the entire group of patients (p= 0.04), in patients with distal tumors, and in old cases. The DNMT3b genotype was not associated with methylation of other genes examined in this study.

Conclusions: Our results suggest that DNMT3b polymorphism is involved in the development of colon cancer and non-random genes promoter methylation among Iranian population.

Keywords: Colorectal cancer; DNMT3B; methylation; polymorphism; tumor suppressor genes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Colorectal Neoplasms / genetics*
  • DNA (Cytosine-5-)-Methyltransferases / genetics*
  • DNA Methylation*
  • DNA Methyltransferase 3B
  • Female
  • Gene Expression
  • Genotyping Techniques
  • Humans
  • Incidence
  • Male
  • Middle Aged
  • Polymerase Chain Reaction
  • Polymorphism, Restriction Fragment Length
  • Polymorphism, Single Nucleotide*
  • Promoter Regions, Genetic / genetics*
  • Risk Factors
  • Sex Factors
  • Young Adult

Substances

  • DNA (Cytosine-5-)-Methyltransferases