The expression of IGF-1R in Helicobacter pylori-infected intestinal metaplasia and gastric cancer.

Abstract:

:Overexpression of IGF-1R has been demonstrated in gastrointestinal cancers, and its expression is reported as the result of the loss of tumor suppressors. IL-16 is involved in the pathophysiological process of chronic inflammatory diseases. The aim of this study is to determine the changes in the expression of IGF-1R in intestinal metaplasia (IM) and gastric cancer (GC) as well as the effect of Helicobacter pylori (H. pylori) and IL-16 on cell proliferation and IGF-1R expression in gastric cells. AGS cells were incubated with combinations of IL-16 and H. pylori. Gastric cell proliferation was studied by BrdU uptake. In H. pylori infected mucosa, IGF-1R was significantly higher in IM than chronic gastritis (CG), and also higher in GC than CG and IM. H. pylori significantly decreased BrdU uptake. IL-16 increased BrdU uptake and IGF-1R on AGS cells which had been decreased by H. pylori. Co-incubation with IL-16 increased the expression of IGF-1R mRNA in H. pylori infected cells. We conclude that the expression of IGF-1R in H. pylori infected gastric mucosa may indicate an early stage of carcinogenesis. The IL-16 secretion by H. pylori can be a trigger for the expression of IGF-1R, and it may also be a factor for gastric carcinogenesis.

journal_name

J Clin Biochem Nutr

authors

Nakajima N,Kozu K,Kobayashi S,Nishiyama R,Okubo R,Akai Y,Moriyama M,Kinukawa N

doi

10.3164/jcbn.16-11

subject

Has Abstract

pub_date

2016-07-01 00:00:00

pages

53-7

issue

1

eissn

0912-0009

issn

1880-5086

pii

jcbn16-11

journal_volume

59

pub_type

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