In colorectal and pancreatic cancer models, this engineered virus induced potent anti-tumor effects via G2/M phase arrest, mediated by p53 phosphorylation and p21 upregulation, while suppressing epithelial-mesenchymal transition (EMT) through downregulation of N-cadherin, vimentin, and α-SMA. Here, ACTA1 is linked to pancreatic neoplasm.