Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 74, Issue 3, Pages 393-398Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-016-2347-2
Keywords
Tumor angiogenesis; Endocytosis; VEGFR2; Signaling; Epsins; Target
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Funding
- NHLBI NIH HHS [R01 HL130845, R01 HL137229, R01 HL093242, R01 HL118676, R01 HL133216] Funding Source: Medline
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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 the 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.
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