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J Proteome Res ; 5(6): 1460-8, 2006 Jun.
Article in English | MEDLINE | ID: mdl-16739997

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.


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