Angiogenesis is not mediated by prostate cancer neuropeptides

J. E. Busby, S. J. Shih, J. C. Yang, Hsing-Jien Kung, Christopher P Evans

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)289-293
Number of pages5
Issue number4
StatePublished - 2003


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

ASJC Scopus subject areas

  • Cancer Research
  • Pathology and Forensic Medicine
  • Clinical Biochemistry
  • Polymers and Plastics


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