Helicobacter pylori infection activates FOS and stress-response genes and alters expression of genes in gastric cancer-specific loci

Genes Chromosomes Cancer. 2004 Aug;40(4):334-41. doi: 10.1002/gcc.20047.

Abstract

We studied human gene expression changes caused by Helicobacter pylori infection by using an in vitro model and 13k cDNA microarrays. A gastric cancer cell line was infected with H. pylori strain NCTC 11637. H. pylori infection was found to induce differential expression of genes in chromosomal locations known to contain frequent chromosomal aberrations and gene mutations specific to gastric cancer. Based on the results of time series experiments, the primary transcription target of the infection seemed to be FOS, the expression of which significantly increased after H. pylori infection. H. pylori infection also activated transcription of several stress-response genes. H. pylori infection may predispose the host cell to DNA damage in the chromosomal locations specific to gastric cancer by activating transcription and promoting histone removal from these sites, thus exposing its target DNA to mutations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chromosome Mapping
  • DNA, Neoplasm / genetics
  • Gene Expression Profiling / methods
  • Gene Expression Regulation, Neoplastic / genetics
  • Gene Expression Regulation, Neoplastic / physiology*
  • Genes, Neoplasm / physiology*
  • Genes, fos / physiology
  • Genetic Markers / genetics*
  • Helicobacter Infections / pathology*
  • Helicobacter pylori / genetics*
  • Helicobacter pylori / immunology
  • Helicobacter pylori / isolation & purification
  • Humans
  • Oligonucleotide Array Sequence Analysis
  • Oncogene Proteins v-fos / physiology*
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / microbiology*
  • Stomach Neoplasms / pathology
  • Stress, Physiological / genetics*

Substances

  • DNA, Neoplasm
  • Genetic Markers
  • Oncogene Proteins v-fos