The CagA protein is delivered into gastric epithelial cells via a type IV secretion system. Once inside the host cells, CagA undergoes tyrosine phosphorylation and interacts with several host cell signaling pathways. These interactions disrupt normal cellular functions, leading to increased cell proliferation, inflammation, and ultimately, oncogenesis. Specifically, CagA can deregulate the Wnt/β-catenin pathway, promote the activation of NF-κB, and interfere with cell adhesion and polarity by interacting with proteins like E-cadherin and SHP-2.
