Abstract
Background Helicobacter pylori has been known as the strongest risk factor in developing gastric carcinoma (GC) through a cascade of epithelial changes that lead to precancerous lesions, which predispose to GC. Aim This study was designed to investigate the expression of P53, SOX2, and SOX9 in H. pylori chronic gastritis, precancerous gastric lesions, and GC. Patients and methods A total of 57 cases of chronic gastritis were selected [37 cases of chronic superficial gastritis without intestinal metaplasia (IM) and 20 cases showed IM], 18 cases of dysplasia, and 30 cases of GC, besides six normal gastric endoscopic biopsies. Giemsa stains were used to detect H. pylori colonies. Immunohistochemical technique was applied to detect P53, SOX2, and SOX9 expression and correlate them with clinicopathological finding. Results Both P53 and SOX9 expressions were statistically increased from normal gastric mucosa through chronic superficial gastritis, IM, dysplastic cases, and GC. In contrast, SOX2 expression was observed in 9.5% of GC, compared with 83.3% of normal mucosa. Among H. pylori-infected cases, P53 expression was found in 53.8% of chronic superficial gastritis, 81.2% of metaplasia, 88.8% of dysplasia, and 80% of GC cases (P 0.05). SOX9 was significantly positively correlated with depth of invasion, grade of the tumor, lymph node metastasis, and distant metastasis of GC (P 0.05). SOX2 was significantly inversely correlated with the grade of the tumor, lymph node metastasis, and distant metastasis. A positive significant was found between P53 and SOX9 in chronic superficial gastritis, IM, dysplasia, and carcinoma cases in relation to H. pylori infection. Conclusion It was elucidated that H. pylori infection can strength and contribute in SOX9 and P53 mutation, considering H. pylori a risk factor for gastric carcinogenesis. It was concluded that SOX2 is able to repress SOX9 and/or P53 expression, which might be one of the molecular mechanisms involved to maintain normal gastric differentiation. SOX9 overexpression and SOX2 suppression that occur in H. pylori infection could lead to IM.
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