Abstract
We investigated the role of Eps8 in pancreatic cancer. Eps8 was significantly increased in pancreatic cancer and colocalized with F-actin, predominantly in pancreatic ductal cells. Eps8 levels were higher in cell lines derived from ascites and metastases than in those from primary tumors. Expression correlated positively with the migratory potential of tumor cells. Eps8 localized to the tips of F-actin filaments, filopodia, and the leading edge of cells. Eps8 knockdown altered cell shape and actin-based cytoskeletal structures, impairing protrusion formation and cell–cell junctions. We concluded that Eps8 is increased in pancreatic cancer and correlates with migratory potential and tumor progression in vitro. Eps8 is essential for actin dynamics and cell interactions, independent of Eps8-like gene products.
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