Dynamic rearrangement of the actin cytoskeleton is a significant hallmark of Helicobacter pylori (H. pylori) infected
gastric epithelial cells leading to cell migration and invasive growth. Considering the cellular mechanisms, the type
IV secretion system (T4SS) and the effector protein cytotoxin-associated gene A (CagA) of H. pylori are well-studied
initiators of distinct signal transduction pathways in host cells targeting kinases, adaptor proteins, GTPases, actin
binding and other proteins involved in the regulation of the actin lattice. In this review, we summarize recent
findings of how H. pylori functionally interacts with the complex signaling network that controls the actin
cytoskeleton of motile and invasive gastric epithelial cells.