Galectin-9 Expression Profile in Patients with Gastric Cancer and Peptic Ulcer Disease

Abstract:
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.
Language:
English
Published:
Research in Molecular Medicine, Volume:4 Issue: 4, Nov 2016
Pages:
1 to 7
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