Screening metatranscriptomes for toxin genes as functional drivers of human colorectal cancer

Bas E. Dutilh, Lennart Backus, Sacha A.F.T. Van Hijum, Harold Tjalsma

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

The colonic mucosa is in constant physical interaction with a dense and complex bacterial community that comprises health-promoting and pathogenic microbes. Here, we highlight important clinical studies and experimental models that have linked the intestinal microbiota to the development of colorectal cancer (CRC). Moreover, we use recently published metatranscriptome sequencing data to test whether potentially carcinogenic toxin genes exhibit higher expression levels in human CRC tissue compared to adjacent non-malignant mucosa. Our analyses show a large variation in expression of toxin(-related) genes from different species. Surprisingly, Enterobacterial toxins were among the highest expressed, while Enterobacteria were not among the most abundant species in these samples. Although we can differentiate on- and off-tumour sites based on toxin reads, the read depth profiles are quite similar and show only limited coverage of the toxin genes. Thus, extended metagenomic studies are needed to obtain a high-resolution picture of host-pathogen interactions during human CRC. © 2013 Elsevier Ltd. All rights reserved.
Original languageEnglish
Pages (from-to)85-99
Number of pages15
JournalBest Practice & Research in Clinical Gastroenterology
Volume27
Issue number1
DOIs
Publication statusPublished - 1 Feb 2013

Keywords

  • Bacterial driver-passenger model
  • Colorectal cancer
  • Enterotoxigenic Bacteroides fragilis
  • Escherichia coli colibactin
  • Metagenomics
  • bacterial toxin
  • fragilysin
  • RNA 16S
  • transcriptome
  • amplicon
  • article
  • colorectal cancer
  • Enterobacteriaceae
  • Escherichia coli
  • gene expression
  • human
  • intestine flora
  • metagenomics
  • microbiome
  • RNA gene

Fingerprint

Dive into the research topics of 'Screening metatranscriptomes for toxin genes as functional drivers of human colorectal cancer'. Together they form a unique fingerprint.

Cite this