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Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression
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Zeitschriftentitel: | Journal of Cancer Research Updates |
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Personen und Körperschaften: | , , , , , , , , , |
In: | Journal of Cancer Research Updates, 2, 2013, 3 |
Format: | E-Article |
Sprache: | Unbestimmt |
veröffentlicht: |
Neoplasia Research
|
author_facet |
Kandice L. Tessneer Xiaofeng Cai Satish Pasula Yunzhou Dong Xiaolei Liu Baojun Chang John McManus Scott Hahn Lili Yu Hong Chen Kandice L. Tessneer Xiaofeng Cai Satish Pasula Yunzhou Dong Xiaolei Liu Baojun Chang John McManus Scott Hahn Lili Yu Hong Chen |
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author |
Kandice L. Tessneer Xiaofeng Cai Satish Pasula Yunzhou Dong Xiaolei Liu Baojun Chang John McManus Scott Hahn Lili Yu Hong Chen |
spellingShingle |
Kandice L. Tessneer Xiaofeng Cai Satish Pasula Yunzhou Dong Xiaolei Liu Baojun Chang John McManus Scott Hahn Lili Yu Hong Chen Journal of Cancer Research Updates Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression |
author_sort |
kandice l. tessneer |
spelling |
Kandice L. Tessneer Xiaofeng Cai Satish Pasula Yunzhou Dong Xiaolei Liu Baojun Chang John McManus Scott Hahn Lili Yu Hong Chen 1929-2279 Neoplasia Research http://dx.doi.org/10.6000/1929-2279.2013.02.03.2 <jats:p>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.</jats:p> Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression Journal of Cancer Research Updates |
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title |
Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression |
title_unstemmed |
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 |
url |
http://dx.doi.org/10.6000/1929-2279.2013.02.03.2 |
publishDate |
2013 |
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<jats:p>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.</jats:p> |
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author | Kandice L. Tessneer, Xiaofeng Cai, Satish Pasula, Yunzhou Dong, Xiaolei Liu, Baojun Chang, John McManus, Scott Hahn, Lili Yu, Hong Chen |
author_facet | Kandice L. Tessneer, Xiaofeng Cai, Satish Pasula, Yunzhou Dong, Xiaolei Liu, Baojun Chang, John McManus, Scott Hahn, Lili Yu, Hong Chen, Kandice L. Tessneer, Xiaofeng Cai, Satish Pasula, Yunzhou Dong, Xiaolei Liu, Baojun Chang, John McManus, Scott Hahn, Lili Yu, Hong Chen |
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description | <jats:p>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.</jats:p> |
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spelling | Kandice L. Tessneer Xiaofeng Cai Satish Pasula Yunzhou Dong Xiaolei Liu Baojun Chang John McManus Scott Hahn Lili Yu Hong Chen 1929-2279 Neoplasia Research http://dx.doi.org/10.6000/1929-2279.2013.02.03.2 <jats:p>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.</jats:p> Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression Journal of Cancer Research Updates |
spellingShingle | Kandice L. Tessneer, Xiaofeng Cai, Satish Pasula, Yunzhou Dong, Xiaolei Liu, Baojun Chang, John McManus, Scott Hahn, Lili Yu, Hong Chen, Journal of Cancer Research Updates, 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 |
title_unstemmed | Epsin Family of Endocytic Adaptor Proteins as Oncogenic Regulators of Cancer Progression |
url | http://dx.doi.org/10.6000/1929-2279.2013.02.03.2 |