Consequence of gastrin-releasing peptide receptor activation in a human colon cancer cell line: a proteomic approach.

Abstract

Gastrin-releasing peptide (GRP) and its receptor (GRPR) are aberrantly up-regulated in colon cancer. When expressed, they act as morphogens, retaining tumor cells in a better differentiated state and retarding metastasis. To identify targets activated in response to GRPR signaling we studied Caco-2 and HT-29 cells, colon cancer cell lines that expresses GRPR as a function of confluence. Total cell protein was extracted from pre-confluent cells (expressing GRP/GRPR) cultured in serum-free media in the presence or absence of GRPR-specific antagonist; as well as from confluent cells that do not express GRPR. Overall, we identified 5 proteins that are specifically down-regulated after GRP/GRPR expression: Bach2, creatine kinase B, p47, and two that could not be identified; and 6 proteins that are up-regulated: gephyrin, HSP70, HP1, ICAM-1, ACAT, and one that could not be identified. These findings suggest that the mechanism(s) by which GRP/GRPR mediate its morphogenic effects in colon cancer involve the actions of a number of hitherto unappreciated proteins.

• Authors: Tom Ruginis, Lauren Taglia, Damien Matusiak, Bao-Shiang Lee, Richard V Benya
• Journal: Journal of proteome research (J Proteome Res) Vol. 5 Issue 6 Pg. 1460-8 (Jun 2006) ISSN: 1535-3893 [Print] United States
• PMID: 16739997 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, Non-P.H.S.)

Chemical References

• Culture Media, Serum-Free
• Proteome
• Receptors, Bombesin
• Gastrin-Releasing Peptide

Topics

• Cell Line, Tumor
• Colonic Neoplasms
• Culture Media, Serum-Free
• Electrophoresis, Gel, Two-Dimensional
• Gastrin-Releasing Peptide (physiology)
• Humans
• Protein Binding
• Proteome (metabolism)
• Receptors, Bombesin (agonists, biosynthesis)
• Signal Transduction
• Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization