Update on molecular pathogenesis of Helicobacter pylori-induced gastric cancer

Table 3 Signaling pathways activated by Helicobacter pylori infection that promote uncontrolled cell proliferation

Signaling pathways	Molecular mechanisms involved in gastric cancer induced by H. pylori
STAT3 pathway	H. pylori activates the STAT3 pathway through upregulation of IL-6, CagA-mediated SHP-2 activation, and TLR2 interaction. STAT3 regulates downstream target genes involved in cellular processes such as development, proliferation, differentiation, EMT, invasion, and metastasis
NF-κB pathway	H. pylori activates NF-κB through direct activation by CagA, IKK kinase, and upregulation of pro-inflammatory factors. NF-κB transcriptionally regulates genes involved in cell cycle progression, apoptosis inhibition, and cross-regulates with other tumor signaling pathways
Wnt/β-catenin	H. pylori activates the Wnt/β-catenin pathway through CagA-mediated accumulation and nuclear translocation of β-catenin. Activation of this pathway disrupts cell cycle regulation, inhibits apoptosis, induces EMT, and promotes tumor cell proliferation, motility, and invasion. Cross-regulation between Wnt/β-catenin and other pathways enhances oncogenic effects
Miscellaneous signaling pathways	H. pylori activates additional signaling pathways including the MAPK pathway (ERK, JNK, p38), PI3K/Akt pathway, Hippo pathway, and various other pathways (HGF/Met, TGF-β, Hedgehog, Notch). These pathways are involved in regulating proliferation, survival, migration, invasion, differentiation, apoptosis, stem cell properties, microRNA map, and exhibit complex cross-regulatory interactions with each other and with the classical pathways

Helicobacter pylori: H. pylori.