Effect of Helicobacterpylori on non-homologous end joining-mediated repair of proximal DNA double-strand breaks in GCV6 cells

Infection with Helicobacter pylori is the strongest known risk factor for gastric cancer, which is one of the leading causes of cancer-related mortality worldwide. H. pylori can contribute to carcinogenesis by inducing the genomic instability of infected cells through increasing accumulation of DNA double-stranded breaks (DSBs) and dereg-ulating DSB repair systems. However, the mechanism of this phenomenon is still being elucidated. This study aims to investigate the impact of H. pylori on the efficacy of non-homologous end joining (NHEJ)-mediated repair of DSB. In this study, we used a human fibroblast cell line bearing a single copy of an NHEJ-reporter substrate stably inserted into the genome, which provides a quantitative measurement of NHEJ. Our results indicated the potential abilities of H. pylori strains to alter the NHEJ-mediated repair of proximal DSB in infected cells. In addition, we found an association between the alteration in the NHEJ efficiency, and the inflammation responses of infected cells caused by H. pylori.

Automated summary

Infection with Helicobacter pylori, a risk factor for gastric cancer, can cause genomic instability in infected cells by increasing DNA double-stranded breaks and disrupting DNA repair systems. This study investigates the impact of H. pylori on the efficacy of non-homologous end joining (NHEJ)-mediated repair of DNA double-strand breaks.