Abstract
The aim of the present study was to investigate an association of genetic polymorphism (rs7521584) located in miR-200a-200b-429 cluster, which has tumor suppressor and pro-inflammatory function, with the development of gastric mucosal atrophy and metaplasia as a pre-malignant condition. Gastric mucosa samples were obtained from the antrum of 393 patients with no malignancies. The rs7521584 genotype was determined using the polymerase chain reaction-single-strand conformation polymorphism analysis method. The degree of gastritis was assessed histologically in all subjects and serum levels of pepsinogen (PG) I/II were quantified in 123 out of 393 patients. Patients with an atrophy score =1 and metaplasia score =1 were classified into the atrophic gastritis group (AG group). The rs7521584 TT genotype was significantly associated with the development of atrophic gastritis [odds ratio (OR), 2.41; 95% confidence interval (CI), 1.10-5.25; P=0.027), particularly in patients with H. pyloriinfection (OR, 3.31; 95% CI, 1.35-8.12; P=0.0089). In addition, in patients younger than 60 years of age, this genotype was associated with atrophic gastritis (OR, 3.15; 95% CI 1.03-9.61; P=0.044)]. In patients with H. pyloriinfection, the metaplasia score was significantly higher in the TT homozygote compared with the GG+GT genotype. In the rs7521584 TT homozygote, serum PG I/II ratio was significantly reduced with increasing age (P=0.0084). No significant trend was identified between the GG+GT genotype and age. The results of the current study indicated that the rs7521584 minor allele homozygote was associated with the development of chronic gastritis under the influence of H. pylori-induced inflammation, particularly with the severity of metaplastic alterations.
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Otsuka, T., Tahara, T., Nakamura, M., Jing, W., Ota, M., Nomura, T., … Arisawa, T. (2018). Polymorphism rs7521584 in miR-429 is associated with the severity of atrophic gastritis in patients with Helicobacter pylori infection. Molecular Medicine Reports, 18(2), 2381–2386. https://doi.org/10.3892/mmr.2018.9200
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