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

Nakajima N, Ito Y, Yokoyama K, Uno A, Kinukawa N, Nemoto N, Moriyama M - J Clin Biochem Nutr (2009)

Bottom Line: 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.In conclusion, the expression of MDM2 in long-term H. pylori infected gastric mucosa may indicate a risk for carcinogenesis.The expression of MDM2 on mucosa can be a mediator for gastric cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology and Hepatology, Nihon University School of Medicine, Tokyo 101-8309, Japan.

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.

No MeSH data available.


Related in: MedlinePlus

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.
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Figure 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.

Mentions: The in vitro study showed that the administration of 10−10, 10−9 M of IL-16 did not influence the BrdU uptake on AGS cells. (AGS only 100 ± 21.97%, 10−10 M IL-16 administration on AGS cells: 95.85 ± 23.90%, 10−9 M IL-16: 102.54 ± 25.77%). But the 105 cfu/ml of H. pylori incubation decreased BrdU uptake on AGS cells (AGS only: 100 ± 21.97% vs. 105 cfu/ml of H. pylori: 85.19 ± 13.57%, p<0.001), 106 cfu/ml of H. pylori infection did not decrease the BrdU uptake on AGS cells (106 cfu/ml of H. pylori: 105.78 ± 22.48%). Further 10−10, and 10−9 M of IL-16 administration increased BrdU uptake on AGS cells which was decreased by 105 cfu/ml of H. pylori infection (105 cfu/ml H. pylori: 85.19 ± 13.57% vs. 105 cfu/ml H.pylori + 10−10 M IL-16: 97.82 ± 15.24%, 105 cfu/ml H.pylori + 10−9 M IL-16: 102.80 ± 14.67%, p<0.001). Also the administration of IL-16 increased BrdU uptake on AGS cells with 106 cfu/ml of H. pylori: (106 cfu/ml H. pylori: 105.78 ± 22.48% vs. 106 cfu/ml H. pylori + 10−10 M IL-16: 143.36 ± 22.65%, 106 cfu/ml H. pylori + 10−9 M IL-16: 120.38 ± 12.62%, p<0.001) (Fig. 3).


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

Nakajima N, Ito Y, Yokoyama K, Uno A, Kinukawa N, Nemoto N, Moriyama M - J Clin Biochem Nutr (2009)

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.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2654476&req=5

Figure 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.
Mentions: The in vitro study showed that the administration of 10−10, 10−9 M of IL-16 did not influence the BrdU uptake on AGS cells. (AGS only 100 ± 21.97%, 10−10 M IL-16 administration on AGS cells: 95.85 ± 23.90%, 10−9 M IL-16: 102.54 ± 25.77%). But the 105 cfu/ml of H. pylori incubation decreased BrdU uptake on AGS cells (AGS only: 100 ± 21.97% vs. 105 cfu/ml of H. pylori: 85.19 ± 13.57%, p<0.001), 106 cfu/ml of H. pylori infection did not decrease the BrdU uptake on AGS cells (106 cfu/ml of H. pylori: 105.78 ± 22.48%). Further 10−10, and 10−9 M of IL-16 administration increased BrdU uptake on AGS cells which was decreased by 105 cfu/ml of H. pylori infection (105 cfu/ml H. pylori: 85.19 ± 13.57% vs. 105 cfu/ml H.pylori + 10−10 M IL-16: 97.82 ± 15.24%, 105 cfu/ml H.pylori + 10−9 M IL-16: 102.80 ± 14.67%, p<0.001). Also the administration of IL-16 increased BrdU uptake on AGS cells with 106 cfu/ml of H. pylori: (106 cfu/ml H. pylori: 105.78 ± 22.48% vs. 106 cfu/ml H. pylori + 10−10 M IL-16: 143.36 ± 22.65%, 106 cfu/ml H. pylori + 10−9 M IL-16: 120.38 ± 12.62%, p<0.001) (Fig. 3).

Bottom Line: 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.In conclusion, the expression of MDM2 in long-term H. pylori infected gastric mucosa may indicate a risk for carcinogenesis.The expression of MDM2 on mucosa can be a mediator for gastric cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology and Hepatology, Nihon University School of Medicine, Tokyo 101-8309, Japan.

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.

No MeSH data available.


Related in: MedlinePlus