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Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression
Tumor angiogenesis, tumor cell proliferation, and tumor cell migration result from an accumulation of oncogenic mutations that alter protein expression and the regulation of various signaling cascades. Epsins, a small family of clathrin-mediated endocytic adaptor proteins, are reportedly upregulated...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3911794/ https://www.ncbi.nlm.nih.gov/pubmed/24501612 http://dx.doi.org/10.6000/1929-2279.2013.02.03.2 |
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author | Tessneer, Kandice L. Cai, Xiaofeng Pasula, Satish Dong, Yunzhou Liu, Xiaolei Chang, Baojun McManus, John Hahn, Scott Yu, Lili Chen, Hong |
author_facet | Tessneer, Kandice L. Cai, Xiaofeng Pasula, Satish Dong, Yunzhou Liu, Xiaolei Chang, Baojun McManus, John Hahn, Scott Yu, Lili Chen, Hong |
author_sort | Tessneer, Kandice L. |
collection | PubMed |
description | Tumor angiogenesis, tumor cell proliferation, and tumor cell migration result from an accumulation of oncogenic mutations that alter protein expression and the regulation of various signaling cascades. Epsins, a small family of clathrin-mediated endocytic adaptor proteins, are reportedly upregulated in a variety of cancers. Importantly, loss of epsins protects against tumorigenesis, thus supporting an oncogenic role for epsins in cancer. Although a clear relationship between epsins and cancer has evolved, the importance of this relationship with regards to cancer progression and anti-cancer therapies remains unclear. In this review, we summarize epsins’ role as endocytic adaptors that modulate VEGF and Notch signaling through the regulated internalization of VEGFR2 and trans-endocytosis of Notch receptors. As both VEGF and Notch signaling have significant implications in angiogenesis, we focus on the newly identified role for epsins in tumor angiogenesis. In addition to epsins’ canonical role in receptor-mediated endocytosis, and the resulting downstream signaling regulation, we discuss the non-canonical role of epsins as regulators of small GTPases and the implications this has on tumor cell proliferation and invasion. Given epsins’ identified roles in tumor angiogenesis, tumor cell proliferation, and tumor cell invasion, we predict that the investigative links between epsins and cancer will provide new insights into the importance of endocytic adaptors and their potential use as future therapeutic targets. |
format | Online Article Text |
id | pubmed-3911794 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
record_format | MEDLINE/PubMed |
spelling | pubmed-39117942014-02-03 Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression Tessneer, Kandice L. Cai, Xiaofeng Pasula, Satish Dong, Yunzhou Liu, Xiaolei Chang, Baojun McManus, John Hahn, Scott Yu, Lili Chen, Hong J Can Res Updates Article Tumor angiogenesis, tumor cell proliferation, and tumor cell migration result from an accumulation of oncogenic mutations that alter protein expression and the regulation of various signaling cascades. Epsins, a small family of clathrin-mediated endocytic adaptor proteins, are reportedly upregulated in a variety of cancers. Importantly, loss of epsins protects against tumorigenesis, thus supporting an oncogenic role for epsins in cancer. Although a clear relationship between epsins and cancer has evolved, the importance of this relationship with regards to cancer progression and anti-cancer therapies remains unclear. In this review, we summarize epsins’ role as endocytic adaptors that modulate VEGF and Notch signaling through the regulated internalization of VEGFR2 and trans-endocytosis of Notch receptors. As both VEGF and Notch signaling have significant implications in angiogenesis, we focus on the newly identified role for epsins in tumor angiogenesis. In addition to epsins’ canonical role in receptor-mediated endocytosis, and the resulting downstream signaling regulation, we discuss the non-canonical role of epsins as regulators of small GTPases and the implications this has on tumor cell proliferation and invasion. Given epsins’ identified roles in tumor angiogenesis, tumor cell proliferation, and tumor cell invasion, we predict that the investigative links between epsins and cancer will provide new insights into the importance of endocytic adaptors and their potential use as future therapeutic targets. 2013-07-01 2013-07-01 /pmc/articles/PMC3911794/ /pubmed/24501612 http://dx.doi.org/10.6000/1929-2279.2013.02.03.2 Text en © 2013 Lifescience Global http://creativecommons.org/licenses/by-nc/3.0/ This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited. |
spellingShingle | Article Tessneer, Kandice L. Cai, Xiaofeng Pasula, Satish Dong, Yunzhou Liu, Xiaolei Chang, Baojun McManus, John Hahn, Scott Yu, Lili Chen, Hong Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression |
title | Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression |
title_full | Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression |
title_fullStr | Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression |
title_full_unstemmed | Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression |
title_short | Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression |
title_sort | epsin family of endocytic adaptor proteins as oncogenic regulators of cancer progression |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3911794/ https://www.ncbi.nlm.nih.gov/pubmed/24501612 http://dx.doi.org/10.6000/1929-2279.2013.02.03.2 |
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