Abstract

Helicobacter pylori (H. pylori) infection is the most common cause of gastric cancer (GC). This microorganism is genetically diverse; GC is caused by several genetic deregulations in addition to environmental factors and bacterial virulence factors. lncRNAs (long noncoding RNAs) are significant biological macromolecules in GC, have specific functions in diseases, and could be therapeutic targets. Altered lncRNAs can lead to the abnormal expression of adjacent protein-coding genes, which may be important in cancer development. Their mechanisms have not been well understood, so we are going to investigate the risk of GC in a population with both high lncRNA and H. pylori infection.

Highlights

  • Helicobacter pylori (H. pylori) is a Gram-negative motile curved microorganism [1] that causes a variety of diseases such as cancer in the gastric mucosa, peptic ulcers, gastritis, and mucosa-associated lymphoid tissue lymphoma (MALT) [2, 3]

  • This review focuses on lncRNAs which are dysregulated in H. pylori-infected gastric cancer (GC) cells [15]

  • These findings show that the NF-κB/miR-2233p/ARID1A axis may cause the process of H. pylori-induced chronic inflammation which leads to gastric cancer and miR223-3p may apply as a target for the intervention of the malignancy [70]

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Summary

Introduction

Helicobacter pylori (H. pylori) is a Gram-negative motile curved microorganism [1] that causes a variety of diseases such as cancer in the gastric mucosa, peptic ulcers, gastritis, and mucosa-associated lymphoid tissue lymphoma (MALT) [2, 3]. The cag pathogenicity island (cag PAI), one of the most important virulence factors of H. pylori, has 31 significant genes, including two regions, cag-I and cag-II [9]. Between these two regions is located an insertion sequence (IS) element, IS605 transposases (tnpA and tnpB); its virulence levels are different [9]. Diet and infection with H. pylori are the most common suspects in gastric tumorigenesis [18]. The occurrence of gastric cancer is a complex process of progressive development that includes multiple factors, multiple steps, and coding and noncoding genes [23]

Coding and Noncoding RNA
Gene Imprinting
X-Inactivation
Autophagy Regulation
Findings
Conclusion and Future Perspectives
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