Welsch Thilo, Endlich Karlhans, Giese Thomas, Büchler Markus W, Schmidt Jan
Department of General, Visceral and Transplantation Surgery, University of Heidelberg, Im Neuenheimer Feld 110, D-69120 Heidelberg, Germany.
Cancer Lett. 2007 Oct 8;255(2):205-18. doi: 10.1016/j.canlet.2007.04.008. Epub 2007 May 29.
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.
我们研究了Eps8在胰腺癌中的作用。Eps8在胰腺癌中显著增加，并与F-肌动蛋白共定位，主要存在于胰腺导管细胞中。源自腹水和转移灶的细胞系中Eps8水平高于源自原发性肿瘤的细胞系。其表达与肿瘤细胞的迁移潜力呈正相关。Eps8定位于F-肌动蛋白丝的末端、丝状伪足以及细胞的前沿。Eps8基因敲低改变了细胞形状和基于肌动蛋白的细胞骨架结构，损害了突起形成和细胞间连接。我们得出结论，Eps8在胰腺癌中增加，并且在体外与迁移潜力和肿瘤进展相关。Eps8对于肌动蛋白动力学和细胞相互作用至关重要，独立于Eps8样基因产物。
