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. 2009 Mar;44(2):196-202.
doi: 10.3164/jcbn.08-254. Epub 2009 Feb 28.

The Expression of Murine Double Minute 2 (MDM2) on Helicobacter pylori-Infected Intestinal Metaplasia and Gastric Cancer

Noriko Nakajima  1 , Yoko Ito, Kiyoshi Yokoyama, Akitake Uno, Noriko Kinukawa, Norimichi Nemoto, Mitsuhiko Moriyama
Affiliations

The Expression of Murine Double Minute 2 (MDM2) on Helicobacter pylori-Infected Intestinal Metaplasia and Gastric Cancer

Noriko Nakajima et al. J Clin Biochem Nutr. 2009 Mar.

Abstract

The overexpression of murine double minute 2 (MDM2) is found in several human tumors, and increased expression of MDM2 inactivates the apoptotic and cell cycle arrest function of p53. Interleukin-16 (IL-16) is a pleiotrophic cytokine and the properties of IL-16 suggest that it involve in the pathophysiological process of chronic inflammatory diseases. In this study, we investigated the expression of MDM2 in intestinal metaplasia and gastric cancer as well as the effect of H. pylori infection and IL-16 on epithelial cell proliferation and MDM2 expression in gastric cells in vitro. The expression of MDM2 on gastric biopsies was studied immunohistochemistry. AGS cells were incubated with a combination of IL-16 and Helicobacter pylori (H. pylori). Gastric epithelial cell proliferation was studied by BrdU uptake and the expressions of MDM2 were studied by ELISA. There was no significant difference on the expression of MDM2 between with and without H. pylori infected chronic gastritis. In H. pylori infected gastric mucosa; the MDM2 expression was higher on intestinal metaplasia and gastric cancer than chronic gastritis. IL-16 administration was increased MDM2 expression and cell proliferation on AGS cells, which was decreased by H. pylori infection. In conclusion, the expression of MDM2 in long-term H. pylori infected gastric mucosa may indicate a risk for carcinogenesis. IL-16 secretion in H. pylori infected mucosa is one of the factors for gastric cancer. The expression of MDM2 on mucosa can be a mediator for gastric cancer.

Keywords: Helicobacter pylori; MDM2; gastric cancer; intestinal metaplasia.

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Figures

Fig. 1
Fig. 1
The expression of MDM2 on gastric mucosa by ABC staining. A. Chronic gastritis, B. Intestinal metaplasia, C. Gastric cancer MDM2 was stained by DAB as brown area.
Fig. 2
Fig. 2
The Expression of MDM2 on H. pylori infected gastric mucosa in chronic gastritis (CG), intestinal metaplasia (IM) and gastric cancer (GC). There was no significant difference on CG between with and without H. pylori infection. But in H. pylori infected mucosa, the expression of MDM2 increased in IM and GC more than CG. (p<0.05)
Fig. 3
Fig. 3
The effect of IL-16 and H. pylori infection on BrdU uptake in AGS cells. The infection of H. pylori decreased BrdU uptake on AGS cells. But further administration of IL-16 increased BrdU uptake on AGS cells which had been decreased by H. pylori infection.
Fig. 4
Fig. 4
The effect of IL-16 and H. pylori infection on MDM2 expression in AGS cells. The infection of H. pylori decreased MDM2 expression on AGS cells, but further administration of IL-16 increased MDM2 expression on AGS cells which had been decreased by H. pylori infection.
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References

    1. Stolte M., Meining A. Helicobacter pylori gastritis of the gastric carcinoma phenotype: Is histology capable of identifying high-risk gastritis? . J. Gastroenterol. 2000;35, Suppl 12:98–101. - PubMed
    1. Haruma K., Kamada T., Ito M., Kitadai Y., Yoshihara M., Sumii K., Kajiyama G. Helicobacter pylori infection is a major risk factor for gastric carcinoma in young patients. Scand. J. Gastroenterol. 2000;35:255–259. - PubMed
    1. Moss S.F., Calam J., Agarwal B., Wang S., Holt P.R. Induction of gastric epithelial apoptosis by Helicobacter pylori. Gut. 1996;38:498–501. - PMC - PubMed
    1. Mannick E.E., Bravo L.E., Zarama G., Realpe J.L., Zhang X.J., Ruiz B., Fontham E.T., Mera R., Miller M.J., Correa P. Inducible nitric oxide synthase, nytrotyrosine, and apoptosis in Helicobacter pylori gastritis: effect of antibiotics and antioxidants. Cancer Res. 1996;56:3238–3243. - PubMed
    1. Peek R.M., Moss S.F., Tham K.T., Pérez-Pérez G.I., Wang S., Miller G.G., Atherton J.C., Holt P.R., Blaser M.J. Helicobacter pylori cagA+ strains and dissociation of gastric epithelial cell proliferation from apoptosis. J. Natl. Cancer Inst. 1997;89:863–868. - PubMed