A lucid review of Helicobacter pylori‐induced DNA damage in gastric cancer

Abstract

Helicobacter pylori (H pylori) is the main risk factor for gastric cancer (GC). In recent years, many studies have addressed the effects of H pylori itself and of H pylori-induced chronic inflammation on DNA damage. Unrepaired or inappropriately repaired DNA damage is one possible carcinogenic mechanism. We may conclude that H pylori-induced DNA damage is one of the carcinogenic mechanisms of GC. In this review, we summarize the interactions between H pylori and DNA damage and the effects of H pylori-induced DNA damage on GC. Then, focusing on oxidative stress, we introduce the application of antioxidants in GC. At the end of this review, we discuss the outlook for further research on H pylori-induced DNA damage. K E Y W O R D SDNA damage, Helicobacter pylori, NF-κB, PLK

Retracted Article: Aclarubicin regulates glioma cell growth and DNA damage through the SIRT1/PI3K/AKT signaling pathway

“…29,30 A constitutive level of endogenous DNA damage, in part, contributes to genomic instability, and is thus involved in tumorigenesis. 31 Multiple evidences have suggested that cellular DNA damage is associated with cell apoptosis. 32,33 A previous study reported that anthracyclines exert anti-cancer activity via inducing DNA damage.…”

Transcriptome profiling implicated in beneficiary actions of kimchi extracts against <i>Helicobacter pylori</i> infection

“…Oxidative stress relevant to pathogenesis of H. pylori infection and associated gastric carcinogenesis, for instance, H. pyloriinduced DNA damages, oncogenic activation via oxidative stress, mitochondrial damages, Nrf2-mediated autophagy, and inflammasome activation, had been proved in many publications, by which antioxidants like vitamin C, vitamin E, and rebamipide had been tried for either enhancing eradication rate or relieving gastric inflammation in animals and human trial. (30)(31)(32)(33)(34)(35)(36)(37) The fact that reactive oxygen species and reactive nitrogen species produced by H. pylori damage the host cells and can result in DNA damage, while H pylori has wisely evolved to keep damaging response, while blunting the host's efforts to kill the bacteria led to the host response that dietary intake of kimchi can serve host to prevent gastric cancer. Conclusively, since oxidative stress in H. pylori infection is defined as an imbalance between excessive production of reactive oxygen and nitrogen species and depletion of antioxidative system to eliminate the reactive intermediates, kimchi significantly enriched antioxidative defense system against chronic H. pylori infection, imposing the importance of adaptive cellular mechanisms involved in disease blocking of H. pylori-associated gastric carcinogenesis.…”

DNA double-strand breaks in the Toxoplasma gondii-infected cells by the action of reactive oxygen species

“…ROS induce oxidative stress, which turns out to cause damages to macromolecules such as DNA, proteins and lipids [25]. Multiple studies have suggested pathogeninduced ROS role in host-cell DNA damage [26][27][28][29][30]. Elevated ROS levels have been reported in T. gondiiinfected host cells [12,31].…”