The intersection of Helicobacter pylori and gastric cancer: signaling pathways and molecular mechanisms

Abstract

Helicobacter pylori (H. pylori) is widely recognized as a potent risk factor for gastric adenocarcinoma, although only a small percentage of infected individuals develop malignancy. Recent advances have provided insights into how H. pylori contributes to gastric tumorigenesis through the modulation of inflammation, DNA damage, and cellular junctions via shared host cell targets and signaling pathways. A thorough examination of the signaling pathways altered by H. pylori infection could facilitate the discovery of previously unidentified infectious causes of cancer. This, in turn, would support the development of preventive strategies for H. pylori-related gastric malignancies by understanding the molecular mechanisms underlying pathogenesis. This review highlights recent advancements in understanding how H. pylori influences host cell signaling pathways to impact inflammation, genomic stability, abnormal cell proliferation, and other biological processes that promote the onset and progression of gastric cancer.