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Nakajima N, Kozu K, Kobayashi S, et al. The expression of IGF-1R in Helicobacter pylori-infected intestinal metaplasia and gastric cancer. J Clin Biochem Nutr. 2016;59(1):53-7doi: 10.3164/jcbn.16-11.
Nakajima, N., Kozu, K., Kobayashi, S., Nishiyama, R., Okubo, R., Akai, Y., Moriyama, M., & Kinukawa, N. (2016). The expression of IGF-1R in Helicobacter pylori-infected intestinal metaplasia and gastric cancer. Journal of clinical biochemistry and nutrition, 59(1), 53-7. https://doi.org/10.3164/jcbn.16-11
Nakajima, Noriko, et al. "The expression of IGF-1R in Helicobacter pylori-infected intestinal metaplasia and gastric cancer." Journal of clinical biochemistry and nutrition vol. 59,1 (2016): 53-7. doi: https://doi.org/10.3164/jcbn.16-11
Nakajima N, Kozu K, Kobayashi S, Nishiyama R, Okubo R, Akai Y, Moriyama M, Kinukawa N. The expression of IGF-1R in Helicobacter pylori-infected intestinal metaplasia and gastric cancer. J Clin Biochem Nutr. 2016 Jul;59(1):53-7. doi: 10.3164/jcbn.16-11. Epub 2016 May 21. PMID: 27499580; PMCID: PMC4933692.
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J Clin Biochem Nutr. 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.

Journal of clinical biochemistry and nutrition

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

Affiliations

  1. Department of Gastroenterology and Hepatology, Nihon University School of Medicine, 1-6 Kandasurugadai, Chiyoda-ku, Tokyo 101-8309, Japan.
  2. Department of Pathology, Nihon University School of Medicine, 1-6 Kandasurugadai, Chiyoda-ku, Tokyo 101-8309, Japan.

PMID: 27499580 PMCID: PMC4933692 DOI: 10.3164/jcbn.16-11

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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