Colon cancer cells: Pro-invasive signalling

• Type: Article in International Scientific Journal
• Date: 2006

Authors

Debruyne, D (Author) Other; Oliveira, MJ (Author) Other; Bracke, M (Author) Other; Mareel, M (Author) Other; Leroy, A (Author) Other

Journal

Title: International Journal of Biochemistry and Cell Biology

Vol. 38

Pages: 1231-1236

ISSN: 1357-2725

Publisher: Elsevier

Indexing

ISI Web of Knowledge - 4 Citations

Scopus - 3 Citations

Other information

Authenticus ID: P-004-Q01

DOI: 10.1016/j.biocel.2006.01.003

Abstract (EN): Colon cancer results from erroneous renewal of the enteric epithelium. Mutations in stem cells, or their proliferative progenitors, cause accumulation of cells that invade into the stroma and continue to divide rather than migrating on top of the basement membrane prior to entering into apoptosis. Many of these changes in invasive activity appear to be related to the invasion-suppressor role of E-cadherin. We have also investigated Listeria monocytogenes and other enteric bacteria, since these bacteria stimulate invasion through the production of a beta-casein-derived 13-amino acid peptide which is produced by enzymes present in the colon cancer ecosystem. The pro-invasive 13-amino acid peptide signals via small guanosine triphosphatases, which modulate the actin cytoskeleton, and via phosphorylation of the delta opioid receptor. The pro-invasive activity of this peptide is neutralized by the delta opioid receptor antagonist, naloxone. Since the delta opioid receptor belongs to the family of G protein-coupled receptors, implicated in colon cancer cell invasion signalling pathways, it is tempting to speculate that opioids could play a role in mediating this trait of malignant tumours.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 6