EGFR Transactivation by Peptide G Protein-Coupled Receptors in Cancer.

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.

journal_name

Curr Drug Targets

journal_title

Current drug targets

authors

Moody TW,Nuche-Berenguer B,Nakamura T,Jensen RT

doi

10.2174/1389450116666150107153609

subject

Has Abstract

pub_date

2016-01-01 00:00:00

pages

520-8

issue

5

eissn

1389-4501

issn

1873-5592

pii

CDT-EPUB-64378

journal_volume

17

pub_type

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