Update on molecular pathogenesis of Helicobacter pylori-induced gastric cancer

Table 1 Key virulence factors involved in Helicobacter pylori infection

Key virulence factors	Mechanisms of action
CagPAI and CagA	CagPAI encodes the type IV secretion system and effector protein CagA. CagA is translocated into epithelial cells, where it phosphorylates and triggers signaling cascades associated with gastric cancer pathogenesis
VacA	VacA is a secreted toxin that induces vacuolation in host cells. It affects T cell proliferation, mitochondrial function, apoptosis, IL-8 release, and autophagy. Genetic polymorphisms in VacA influence its activity and are associated with the risk of gastric cancer
Urease	Urease hydrolyzes urea to neutralize stomach acid and maintain an optimal pH for bacterial survival
Flagella	Flagella facilitate bacterial movement and colonization. They also contribute to biofilm formation and modulate the immune response by inducing the release of IL-8
Outer membrane proteins (OMPs)	OMPs like BabA, SabA, and OipA interact with host receptors, promoting long-term colonization, chronic inflammation, and IL-8 secretion

CagA: Cytotoxin-associated gene A; BabA: Blood group antigen-binding adhesion A; SabA: Sialic acid-binding adhesion A; VacA: Vacuolating cytotoxin gene A; IL: Interleukin.