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. 2016 Jul;59(1):53-7.
doi: 10.3164/jcbn.16-11. Epub 2016 May 21.

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

Noriko Nakajima  1 , Karina Kozu  1 , Shun Kobayashi  1 , Ryu Nishiyama  1 , Rie Okubo  1 , Yuichi Akai  1 , Mitsuhiko Moriyama  1 , Noriko Kinukawa  2
Affiliations

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

Noriko Nakajima et al. J Clin Biochem Nutr. 2016 Jul.

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.

Keywords: Helicobacter pylori; IGF-1R; chronic gastritis; gastric cancer; intestinal metaplasia.

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Figures

Fig. 1
Fig. 1
The expression of IGF-1R on gastric mucosa of chronic gastritis and gastric cancer by ABC staining. IGF-1R was staining by DAB as brown area.
Fig. 2
Fig. 2
The expression of IGF-1R on gastric mucosa. There was no significant difference between with and without H. pylori infection on chronic gastritis. The expression of IGF-1R was significantly increased in intestinal metaplasia and gastric cancer than chronic gastritis.
Fig. 3
Fig. 3
The effect of H. pylori and IL-16 on BrdU uptake on AGS cells. H. pylori infection decreased the BrdU uptake of AGS cells. The administration of IL-16 significantly increased the BrdU uptake on AGS cells which was decreased by H. pylori infection.
Fig. 4
Fig. 4
The effect of H. pylori and IL-16 on IGF-1R protein levels of AGS cells. H. pylori infection decreased the expression of IGF-1R protein of AGS cells. The administration of IL-16 significantly increased the expressions of IGF-1R protein which was decreased by H. pylori infection.
Fig. 5
Fig. 5
The effect of H. pylori and IL-16 on the expression of IGF-1R mRNA of AGS cells. H. pylori infection decreased the expression of IGF-1R mRNA of AGS cells. The administration of IL-16 significantly increased the expressions of IGF-1R mRNA which was decreased by H. pylori infection.
See this image and copyright information in PMC

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