Published online Nov 6, 2022. doi: 10.12998/wjcc.v10.i31.11283
Peer-review started: July 7, 2022
First decision: July 31, 2022
Revised: August 14, 2022
Accepted: September 6, 2022
Article in press: September 6, 2022
Published online: November 6, 2022
Processing time: 112 Days and 3.7 Hours
Helicobacter pylori (H. pylori) is a Gram-negative bacterium that infects about half of the world's population. H. pylori infection prevails by several mechanisms of adaptation of the bacteria and by its virulence factors including the cytotoxin associated antigen A (CagA). CagA is an oncoprotein that is the protagonist of gastric carcinogenesis associated with prolonged H. pylori infection. In this sense, small regulatory RNAs (sRNAs) are important macromolecules capable of inhibiting and activating gene expression. This function allows sRNAs to act in adjusting to unstable environmental conditions and in responding to cellular stresses in bacterial infections. Recent discoveries have shown that nickel-regulated small RNA (NikS) is a post-transcriptional regulator of virulence properties of H. pylori, including the oncoprotein CagA. Notably, high concentrations of nickel cause the reduction of NikS expression and consequently this increases the levels of CagA. In addition, NikS expression appears to be lower in clinical isolates from patients with gastric cancer when compared to patients without. With that in mind, this minireview approaches, in an accessible way, the most important and current aspects about the role of NikS in the control of virulence factors of H. pylori and the potential clinical repercussions of this modulation.
Core Tip: This paper aims to review current information about the role of nickel-regulated small RNA (NikS) in the modulation of main Helicobacter pylori virulence factors, specially cytotoxin associated antigen A (CagA), which is crucial to gastric cancer development. Here we explore what is the most important about the epigenetic processes involved in the interaction between nickel levels, NikS, and CagA and their potential clinical repercussions.