AI Article Synopsis

  • Gastrin-releasing peptide (GRP) and its receptor (GRPR) are found to be overly expressed in colon cancer, where they help keep tumor cells better differentiated and slow down their spread.
  • Research on colon cancer cell lines Caco-2 and HT-29 identified changes in protein levels in response to GRPR signaling, revealing specific proteins that were both down-regulated and up-regulated based on GRP/GRPR expression.
  • A total of 11 proteins were identified as being significantly affected by GRP/GRPR signaling, indicating that there are important, previously less recognized proteins involved in how GRP/GRPR influence colon cancer behavior.

Article 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.

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http://dx.doi.org/10.1021/pr060005gDOI Listing

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