IGF-1 and its receptor in esophageal cancer: association with adenocarcinoma and visceral obesity

Type Article

Journal Article

Authors

S. L. Doyle; C. L. Donohoe; S. P. Finn; J. M. Howard; F. E. Lithander; J. V. Reynolds; G. P. Pidgeon; J. Lysaght

Year of publication

2012

Publication/Journal

Am J Gastroenterol

Volume

107

Issue

2

Pages

196-204

Abstract

OBJECTIVES: The insulin-like growth factor (IGF) pathway and visceral obesity have been independently linked with esophageal cancer. This study aimed to delineate the differential and interlinked role of visceral obesity and the IGF-1 system in esophageal adenocarcinoma and esophageal squamous-cell carcinoma (SCC). METHODS: IGF-1 receptor (IGF-1R) mRNA and protein were examined in esophageal SCC (KYSE 410, OE21) and esophageal adenocarcinoma (OE19, OE33) cell lines by western blotting. Tumor cell proliferation in response to IGF-1 was assessed by bromodeoxyuridine incorporation assay. In esophageal tumor sections, expression of IGF-1R and CD68(+) cell numbers were assessed by immunohistochemistry. IGF-1 was measured in serum from esophageal cancer patients, Barrett's esophagus patients, and healthy controls by enzyme-linked immunosorbent assay. RESULTS: Higher IGF-1R protein expressions were observed in SCC cells compared with esophageal adenocarcinoma cells however only adenocarcinoma cell lines significantly increased proliferation in response to IGF-1 (P