Activation of the DNA damage response pathway in the infected gastric tissue with Helicobacter pylori: a case-control study

• Published in: Journal of infection in developing countries Vol. 17; no. 8; pp. 1125 - 1129
• Main Authors: Rajaei, Amiratabak, Ghameshlou, Armin, Shirkoohi, Reza, Shakoori Farahani, Abbas, Mirbagheri, Seyedeh Zohre, Bakhtiari, Ronak, Haeri, Melika Sadat, Rashidi-Nezhad, Ali, Alebouyeh, Masoud
• Format: Journal Article
• Language: English
• Published: 31.08.2023
• ISSN: 1972-2680; 1972-2680
• DOI: 10.3855/jidc.17655

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 pre-cancerous gastric tissue.