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Activation of the Dna Damage Response Pathway in the Infected Gastric Tissue With Helicobacter Pylori: A Case-Control Study Publisher Pubmed



Rajaei A1 ; Ghameshlou A1 ; Shirkoohi R2, 3 ; Farahani AS3 ; Mirbagheri S4 ; Bakhtiari R4 ; Haeri MS1 ; Rashidinezhad A3, 5 ; Alebouyeh M6
Authors
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Authors Affiliations
  1. 1. Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
  2. 2. Molecular Genetic Department, Cancer Research Center, Cancer Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Genetic Ward, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Pathobiology, School of Public Health and Institute Health Research, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Maternal, Fetal and Neonatal Research Center, family health research institute, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Pediatric Infections Research Center, Research Institute for Children's Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Source: Journal of Infection in Developing Countries Published:2023


Abstract

Introduction: Gastritis is among the most common human diseases worldwide. Although the involvement of Helicobacter pylori infection as a class I human carcinogen for gastric cancer progression is accepted, it is not well known how gastritis progression to atrophy and stomach cancer occurs. In this case-control study, the potential link of H. pylori infection with alteration in the transcription of genes involved in DNA Damage Response pathways was investigated among the patients with gastritis. Methodology: To measure the difference in the relative mRNA expression level of ATM, CHEK2, TP53, DCLRE1C, POLM, and XRCC4 genes between H. pylori-infected and non-infected patients, gastric biopsies of 30 H. pylori infected patients with moderate chronic gastritis and 30 non-infected patients with mild chronic gastritis were analyzed. Results: Up-regulation of genes linked to non-homologous end joining (NHEJ) pathway (DCLRE1C, POLM, and XRCC) was shown in 40% (8.44 fold ± 13.91), 63.33% (15.72 fold ± 33.08) and 50% (9.99 fold ± 21.55), respectively, and also to DDR pathway (ATM, CHEK2, and TP53) in 33% (2.42 fold ± 3.17), 40% (2.86 fold ± 3.61) and 50% (5.00 fold ± 6.52), respectively. No correlation was detected between alteration in the transcription level of the studied genes and age or gender. Conclusions: Our results provide new data that may support the potential involvement of H. pylori infection in the activation of genes involved in DNA damage response, mainly through a non-homologous end-joining DNA repair system that might be linked to mutagenesis in the precancerous gastric tissue. Copyright © 2023 Rajaei et al. This is an open-access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.