EGFR Transactivation by Peptide G Protein-Coupled Receptors in Cancer

Author(s): Terry W. Moody, Bernardo Nuche-Berenguer, Taichi Nakamura, Robert T. Jensen.

Journal Name: Current Drug Targets

Volume 17 , Issue 5 , 2016

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Abstract:

Lung cancer kills approximately 1.3 million citizens in the world annually. The tyrosine kinase inhibitors (TKI) erlotinib and gefitinib are effective anti-tumor agents especially in lung cancer patients with epidermal growth factor receptor (EGFR) mutations. The goal is to increase the potency of TKI in lung cancer patients with wild type EGFR. G protein-coupled receptors (GPCR) transactivate the wild type EGFR in lung cancer cells. The GPCR can be activated by peptide agonists causing phosphatidylinositol turnover or stimulation of adenylylcyclase. Recently, nonpeptide antagonists were found to inhibit the EGFR transactivation caused by peptides. Nonpeptide antagonists for bombesin (BB), neurotensin (NTS) and cholecystokinin (CCK) inhibit lung cancer growth and increase the cytotoxicity of gefitinib. The results suggest that GPCR transactivation of the EGFR may play an important role in cancer cell proliferation.

Keywords: Epidermal growth factor receptor, G protein-coupled receptor, lung cancer, non-peptide receptor antagonists, peptide receptor agonists, transactivation of tyrosine kinase receptors.

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Article Details

VOLUME: 17
ISSUE: 5
Year: 2016
Page: [520 - 528]
Pages: 9
DOI: 10.2174/1389450116666150107153609
Price: $58

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