ACTA1 and cancer: This highly invasive phenotype may be attributed to the dysregulation of EMT in G.C. EMT encompasses a complex cellular process in which gastric epithelial cells acquire mesenchymal characteristics and lose epithelial traits, including the crucial E-cadherin, as well as the upregulation of matrix metalloproteinases (MMPs), vimentin, and α-smooth muscle actin (α-SMA), all contributing to enhanced cancer invasion and metastasis.