Volume 4, Issue 4 (Nov 2016)                   Res Mol Med (RMM) 2016, 4(4): 1-7 | Back to browse issues page


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Naghavi-Alhosseini M, Taghvaei T, Asgarian-Omran H. Galectin-9 Expression Profile in Patients with Gastric Cancer and Peptic Ulcer Disease. Res Mol Med (RMM) 2016; 4 (4) :1-7
URL: http://rmm.mazums.ac.ir/article-1-217-en.html
1- Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
2- Department of Internal Medicine, Imam Khomeini Hospital, Mazandaran University of Medical Sciences, Sari, Iran
3- Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran , asgarianhossein@yahoo.com
Abstract:   (6044 Views)

Background: Chronic inflammation and dys-regulation of the immune system mechanisms are now well established as primary triggers of gastric cancer and peptic ulcer disease. Galectin-9 (Gal-9) is a member of the galectin family and known as an inducer of cell aggregation, adhesion and apoptosis. Gal-9 interaction with its main ligand T-cell immunoglobulin and mucin domain protein-3 (Tim-3) leads to the apoptosis of T cells and dys-regulation of the immune responses in different tumors. In the current study, the mRNA expression pattern of Gal-9 was evaluated in gastric biopsies of patients with gastric cancer and peptic ulcer disease.

Methods: In this case control study, gastric biopsies were obtained from 46 patients with gastric cancer, 44 patients with peptic ulcer disease and 41 cases with non-ulcer dyspepsia served as controls who underwent endoscopy for evaluation of their gastric problems. Infection with Helicobacter pylori was determined by rapid urease test for all participants and H&E staining for GC patients. Total RNA was extracted from all gastric tissues and used for cDNA synthesis. Relative expression of Gal-9 mRNA was determined by Real-Time PCR using β-actin as a housekeeping gene.

Results: Gal-9 was similarly expressed in all three studied groups. No statistical difference was found for Gal-9 expression between gastric cancer patients and control group (2-ΔCt =0.022 vs 0.0144, p=0.30) and also between peptic ulcer and control groups (2-ΔCt =0.088 vs 0.144, p=0.16). No correlation was found for Gal-9 expression and infection with Helicobacter pylori (2-ΔCt = 0.1 vs 0.129, p=0.51).

Conclusion: Similar expression of Gal-9 in gastric tissues from patients with gastric cancer, peptic ulcer and also non-ulcer dyspepsia individuals suggest no possible role of this molecule on tumorigenesis and immunoregulatory mechanisms of these gastric disorders.

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Type of Study: Research | Subject: Immunology
Published: 2016/12/31

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