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

Samuel Myllykangas, Outi Monni, Bálint Nagy, Hilpi Rautelin, Sakari Knuutila

Research output: Contribution to journalArticle

12 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)334-341
Number of pages8
JournalGenes Chromosomes and Cancer
Volume40
Issue number4
DOIs
Publication statusPublished - Aug 1 2004

ASJC Scopus subject areas

  • Genetics
  • Cancer Research

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