E. coli and colon cancer: is mutY a culprit?

Cancer Lett. 2013 Dec 1;341(2):127-31. doi: 10.1016/j.canlet.2013.08.003. Epub 2013 Aug 7.

Abstract

The recent demonstration of a role of Escherichia coli in the development of invasive carcinoma in mice ushers a new era of bacterial involvement in cancer etiology. It has been shown previously that the colonic mucosa of colorectal carcinoma (CRC) is exclusively colonized by intracellular E. coli instead of extracellular form found in normal colonic mucosa. Surprisingly, the DNA repair gene MUTYH, which is a homologue of the E. coli gene mutY, is responsible for CRC. The current paper discusses the potential role of mutY in CRC etiology and concludes that research in this area can bring together the diverse threads of the CRC etiology puzzle.

Keywords: Carcinogenesis; Chronic inflammation; E. coli; MUTYH; mutY.

Publication types

  • Review

MeSH terms

  • Animals
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / microbiology
  • Colorectal Neoplasms / pathology
  • DNA Glycosylases / genetics*
  • DNA Glycosylases / metabolism
  • DNA Repair / genetics
  • Escherichia coli / genetics*
  • Escherichia coli / physiology
  • Escherichia coli Proteins / genetics*
  • Escherichia coli Proteins / metabolism
  • Host-Pathogen Interactions / genetics
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / microbiology
  • Intestinal Mucosa / pathology
  • Mice
  • Models, Genetic

Substances

  • Escherichia coli Proteins
  • DNA Glycosylases
  • mutY adenine glycosylase