Angiogenesis is not mediated by prostate cancer neuropeptides
Angiogenesis is not mediated by prostate cancer neuropeptides
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DOI：
10.1023/b:agen.0000029409.94626.64
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发表时间：
2003-01-01
期刊：
影响因子：
9.8
通讯作者：
Evans, C. P.
中科院分区：
文献类型：
--
作者：
Busby, J. E.;Shih, S.-J.;Evans, C. P.
一旦转移，前列腺癌（CaP）的治疗选择仅限于雄激素戒断。在这种环境中，细胞通常发展成雄激素非依赖性状态，导致患者死亡。已经表明，在这种转变过程中，CaP细胞转分化为产生神经肽的神经内分泌细胞。这些神经肽对周围的CaP细胞具有促有丝分裂作用。以前的观察表明，内皮细胞可能显示出类似的促有丝分裂反应的神经肽，牵连血管生成的进展钙磷。我们刺激人脐静脉内皮细胞（HUVEC）与神经肽蛙皮素和神经降压素和测量增殖，迁移，细胞管的形成，和酪氨酸激酶激活。在我们的研究中，神经降压素和蛙皮素没有刺激HUVEC增殖，迁移，也没有管形成。虽然HUVEC表达非受体酪氨酸激酶Fak、Src和Etk，其介导CaP中的神经肽信号传导，但它们不被HUVEC中的神经肽激活。
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.