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Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression
Epsins have an important role in mediating clathrin-mediated endocytosis of ubiquitinated cell surface receptors. The potential role for epsins in tumorigenesis and cancer metastasis by regulating intracellular signaling pathways has largely not been explored. Epsins are reportedly upregulated in se...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3649151/ https://www.ncbi.nlm.nih.gov/pubmed/23691361 http://dx.doi.org/10.1155/2013/420597 |
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author | Tessneer, Kandice L. Pasula, Satish Cai, Xiaofeng Dong, Yunzhou Liu, Xiaolei Yu, Lili Hahn, Scott McManus, John Chen, Yiyuan Chang, Baojun Chen, Hong |
author_facet | Tessneer, Kandice L. Pasula, Satish Cai, Xiaofeng Dong, Yunzhou Liu, Xiaolei Yu, Lili Hahn, Scott McManus, John Chen, Yiyuan Chang, Baojun Chen, Hong |
author_sort | Tessneer, Kandice L. |
collection | PubMed |
description | Epsins have an important role in mediating clathrin-mediated endocytosis of ubiquitinated cell surface receptors. The potential role for epsins in tumorigenesis and cancer metastasis by regulating intracellular signaling pathways has largely not been explored. Epsins are reportedly upregulated in several types of cancer including human skin, lung, and canine mammary cancers. However, whether their expression is elevated in prostate cancer is unknown. In this study, we investigated the potential role of epsins in prostate tumorigenesis using the wild type or epsin-deficient human prostate cancer cells, LNCaP, in a human xenograft model, and the spontaneous TRAMP mouse model in wild type or epsin-deficient background. Here, we reported that the expression of epsins 1 and 2 is upregulated in both human and mouse prostate cancer cells and cancerous tissues. Consistent with upregulation of epsins in prostate tumors, we discovered that depletion of epsins impaired tumor growth in both the human LNCaP xenograft and the TRAMP mouse prostate. Furthermore, epsin depletion significantly prolonged survival in the TRAMP mouse model. In summary, our findings suggest that epsins may act as oncogenic proteins to promote prostate tumorigenesis and that depletion or inhibition of epsins may provide a novel therapeutic target for future prostate cancer therapies. |
format | Online Article Text |
id | pubmed-3649151 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-36491512013-05-20 Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression Tessneer, Kandice L. Pasula, Satish Cai, Xiaofeng Dong, Yunzhou Liu, Xiaolei Yu, Lili Hahn, Scott McManus, John Chen, Yiyuan Chang, Baojun Chen, Hong ISRN Oncol Research Article Epsins have an important role in mediating clathrin-mediated endocytosis of ubiquitinated cell surface receptors. The potential role for epsins in tumorigenesis and cancer metastasis by regulating intracellular signaling pathways has largely not been explored. Epsins are reportedly upregulated in several types of cancer including human skin, lung, and canine mammary cancers. However, whether their expression is elevated in prostate cancer is unknown. In this study, we investigated the potential role of epsins in prostate tumorigenesis using the wild type or epsin-deficient human prostate cancer cells, LNCaP, in a human xenograft model, and the spontaneous TRAMP mouse model in wild type or epsin-deficient background. Here, we reported that the expression of epsins 1 and 2 is upregulated in both human and mouse prostate cancer cells and cancerous tissues. Consistent with upregulation of epsins in prostate tumors, we discovered that depletion of epsins impaired tumor growth in both the human LNCaP xenograft and the TRAMP mouse prostate. Furthermore, epsin depletion significantly prolonged survival in the TRAMP mouse model. In summary, our findings suggest that epsins may act as oncogenic proteins to promote prostate tumorigenesis and that depletion or inhibition of epsins may provide a novel therapeutic target for future prostate cancer therapies. Hindawi Publishing Corporation 2013-04-04 /pmc/articles/PMC3649151/ /pubmed/23691361 http://dx.doi.org/10.1155/2013/420597 Text en Copyright © 2013 Kandice L. Tessneer et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Tessneer, Kandice L. Pasula, Satish Cai, Xiaofeng Dong, Yunzhou Liu, Xiaolei Yu, Lili Hahn, Scott McManus, John Chen, Yiyuan Chang, Baojun Chen, Hong Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression |
title | Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression |
title_full | Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression |
title_fullStr | Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression |
title_full_unstemmed | Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression |
title_short | Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression |
title_sort | endocytic adaptor protein epsin is elevated in prostate cancer and required for cancer progression |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3649151/ https://www.ncbi.nlm.nih.gov/pubmed/23691361 http://dx.doi.org/10.1155/2013/420597 |
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