Eps8 is increased in pancreatic cancer and required for dynamic actin-based cell protrusions and intercellular cytoskeletal organization

被引：67

作者：

Welsch, Thilo

Endlich, Karlhans

Giese, Thomas

Buechler, Markus W.

Schmidt, Jan

机构：

[1] Heidelberg Univ, Dept Gen Visceral & Transplant Surg, D-69120 Heidelberg, Germany

[2] Ernst Moritz Arndt Univ Greifswald, Dept Anat & Cell Biol, D-17487 Greifswald, Germany

[3] Heidelberg Univ, Dept Immunol, D-6900 Heidelberg, Germany

来源：

CANCER LETTERS | 2007年 / 255卷 / 02期

关键词：

Eps8; actin; migration; pancreatic cancer; cell protrusion;

D O I：

10.1016/j.canlet.2007.04.008

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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. EpsS is essential for actin dynamics and cell interactions, independent of Eps8-like gene products. (c) 2007 Elsevier Ireland Ltd. All rights reserved.

引用

收藏

页码：205 / 218

页数：14

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