Genome-wide screening of genes regulated by DNA methylation in colon cancer development

PLoS One. 2012;7(10):e46215. doi: 10.1371/journal.pone.0046215. Epub 2012 Oct 1.

Abstract

Tumorigenesis is accompanied by changes in the DNA methylation pattern. Our aim was to test a novel approach for identification of transcripts at whole transcript level which are regulated by DNA methylation. Our approach is based on comparison of data obtained from transcriptome profiling of primary human samples and in vitro cell culture models. Epithelial cells were collected by LCM from normal, adenoma, and tumorous colonic samples. Using gene expression analysis, we identified downregulated genes in the tumors compared to normal tissues. In parallel 3000 upregulated genes were determined in HT-29 colon adenocarcinoma cell culture model after DNA demethylation treatment. Of the 2533 transcripts showing reduced expression in the tumorous samples, 154 had increased expression as a result of DNA demethylation treatment. Approximately 2/3 of these genes had decreased expression already in the adenoma samples. Expression of five genes (GCG, NMES-1, LRMP, FAM161B and PTGDR), was validated using RT-PCR. PTGDR showed ambiguous results, therefore it was further studied to verify the extent of DNA methylation and its effect on the protein level. Results confirmed that our approach is suitable for genome-wide screening of genes which are regulated or inactivated by DNA methylation. Activity of these genes possibly interferes with tumor progression, therefore genes identified can be key factors in the formation and in the progression of the disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics*
  • Adenocarcinoma / metabolism*
  • Colonic Neoplasms / genetics*
  • Colonic Neoplasms / metabolism*
  • DNA Methylation / genetics
  • DNA Methylation / physiology*
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic / genetics
  • Gene Expression Regulation, Neoplastic / physiology*
  • Genome, Human / genetics*
  • Humans
  • Immunohistochemistry
  • Membrane Proteins / metabolism
  • Microarray Analysis
  • Neoplasm Proteins / metabolism
  • Nuclear Proteins / metabolism
  • Principal Component Analysis
  • Receptors, Immunologic / metabolism
  • Receptors, Prostaglandin / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Cells, Cultured

Substances

  • IRAG2 protein, human
  • Membrane Proteins
  • Neoplasm Proteins
  • Nuclear Proteins
  • Receptors, Immunologic
  • Receptors, Prostaglandin
  • c15orf48 protein, human
  • prostaglandin D2 receptor

Grants and funding

This study was supported by the National Office for Research and Technology, Hungary (TECH_08-A1/2-2008- 0114 grant), by the Hungarian National Innovation Office, and by the Danish National Research Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.