Endothelial epsins as regulators and potential therapeutic targets of tumor angiogenesis.
Endothelial epsins as regulators and potential therapeutic targets of tumor angiogenesis.
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内皮蛋白酶作为肿瘤血管生成的调节剂和潜在治疗靶点。
DOI：
10.1007/s00018-016-2347-2
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发表时间：
2017-02
期刊：
影响因子：
--
通讯作者：
Chen H
中科院分区：
文献类型：
--
作者：
Song K;Wu H;Rahman HN;Dong Y;Wen A;Brophy ML;Wong S;Kwak S;Bielenberg DR;Chen H
VEGF驱动的肿瘤血管生成已被证实为几种肿瘤类型的中心靶点，值得持续和进一步考虑，以提高目前治疗模式的疗效和选择性。Epsins是一个内吞网格蛋白衔接子家族，参与调节内皮细胞VEGFR2信号传导，其失活导致非生产性渗漏性新血管生成，因此阻碍肿瘤发生和进展。靶向内皮epsins具有特殊的意义，因为它不影响其他血管生成信号通路或破坏正常的静止血管，这表明选择性调节肿瘤血管生成。这篇综述强调了内皮epsins在肿瘤血管生成中的关键作用及其潜在的分子事件，以及利用这些新理解的机制来禁止内源性内皮epsins的正常功能的策略。
VEGF-driven tumor angiogenesis has been validated as a central target in several tumor types deserving of continuous and further considerations to improve the efficacy and selectivity of current therapeutic paradigms. Epsins, a family of endocytic clathrin adaptors, have been implicated in regulating endothelial cell VEGFR2 signaling, where its inactivation leads to nonproductive leaky neo-angiogenesis and therefore impedes tumor development and progression. Targeting endothelial epsins is of special significance due to its lack of affecting other angiogenic signaling pathways or disrupting normal quiescent vessels, suggesting a selective modulation of tumor angiogenesis. This review highlights seminal findings on the critical role of endothelial epsins in tumor angiogenesis and their underlying molecular events, as well as strategies to prohibit the normal function of endogenous endothelial epsins that capitalize on these newly understood mechanisms.