Angiogenesis is not mediated by prostate cancer neuropeptides

被引：8

作者：

J.E. Busby

S.-J. Shih

J.C. Yang

H.-J. Kung

C.P. Evans

机构：

[1] Department of Urology, University of California, Davis, School of Medicine, Sacramento, CA

[2] Department of Biological Chemistry, University of California, Davis, School of Medicine, Sacramento, CA

[3] Department of Urology, University of California, Davis School of Medicine, Sacramento, CA 95817

来源：

Angiogenesis | 2003年 / 6卷 / 4期

关键词：

Angiogenesis; Endothelial cell; Neuroendocrine; Neuropeptides; Neurotrophins; Non-receptor tyrosine kinases; Prostate cancer; Signal transduction;

D O I：

10.1023/B:AGEN.0000029409.94626.64

中图分类号：

学科分类号：

摘要：

Once metastatic, prostate cancer (CaP) treatment options are limited to androgen withdrawal. In this environment, the cells often develop an androgen independent state resulting in patient demise. It has been shown that during this transition, CaP cells transdifferentiate to neuroendocrine cells, which produce neuropeptides. These neuropeptides have a mitogenic effect on surrounding CaP cells. Previous observations suggest that endothelial cells may show a similar mitogenic response to neuropeptides, implicating angiogenesis in the progression of CaP. We stimulated human umbilical endothelial cells (HUVECs) with the neuropeptides bombesin and neurotensin and measured proliferation, migration, cell tube formation, and tyrosine kinase activation. In our studies, neurotensin and bombesin did not stimulate HUVEC proliferation, migration, nor tube formation. Although HUVECs express the non-receptor tyrosine kinases Fak, Src, and Etk which mediate neuropeptide signaling in CaP, they are not activated by neuropeptides in HUVECs.

引用

页码：289 / 293

页数：4

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