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The Emerging Regulation of VEGFR-2 in Triple-Negative Breast Cancer

Vascular endothelial growth factor-A (VEGF) signals vascular development and angiogenesis mainly by binding to VEGF receptor family member 2 (VEGFR-2). Adaptor proteins mediate many VEGFR-2’s functions in the development of blood vessels. Cancer cells secrete VEGF to activate VEGFR-2 pathway in thei...

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Detalles Bibliográficos
Autores principales: Zhu, Xiaoxia, Zhou, Wen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598588/
https://www.ncbi.nlm.nih.gov/pubmed/26500608
http://dx.doi.org/10.3389/fendo.2015.00159
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author Zhu, Xiaoxia
Zhou, Wen
author_facet Zhu, Xiaoxia
Zhou, Wen
author_sort Zhu, Xiaoxia
collection PubMed
description Vascular endothelial growth factor-A (VEGF) signals vascular development and angiogenesis mainly by binding to VEGF receptor family member 2 (VEGFR-2). Adaptor proteins mediate many VEGFR-2’s functions in the development of blood vessels. Cancer cells secrete VEGF to activate VEGFR-2 pathway in their neighboring endothelial cells in the process of cancer-related angiogenesis. Interestingly, activation of VEGFR-2 signaling is found in breast cancer cells, but its role and regulation are not clear. We highlighted research advances of VEGFR-2, with a focus on VEGFR-2’s regulation by mutant p53 in breast cancer. In addition, we reviewed recent Food and Drug Administration-approved tyrosine kinase inhibitor drugs that can inhibit the function of VEGFR-2. Ongoing preclinical and clinical studies might prove that pharmaceutically targeting VEGFR-2 could be an effective therapeutic strategy in treating triple-negative breast cancer.
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spelling pubmed-45985882015-10-23 The Emerging Regulation of VEGFR-2 in Triple-Negative Breast Cancer Zhu, Xiaoxia Zhou, Wen Front Endocrinol (Lausanne) Endocrinology Vascular endothelial growth factor-A (VEGF) signals vascular development and angiogenesis mainly by binding to VEGF receptor family member 2 (VEGFR-2). Adaptor proteins mediate many VEGFR-2’s functions in the development of blood vessels. Cancer cells secrete VEGF to activate VEGFR-2 pathway in their neighboring endothelial cells in the process of cancer-related angiogenesis. Interestingly, activation of VEGFR-2 signaling is found in breast cancer cells, but its role and regulation are not clear. We highlighted research advances of VEGFR-2, with a focus on VEGFR-2’s regulation by mutant p53 in breast cancer. In addition, we reviewed recent Food and Drug Administration-approved tyrosine kinase inhibitor drugs that can inhibit the function of VEGFR-2. Ongoing preclinical and clinical studies might prove that pharmaceutically targeting VEGFR-2 could be an effective therapeutic strategy in treating triple-negative breast cancer. Frontiers Media S.A. 2015-10-09 /pmc/articles/PMC4598588/ /pubmed/26500608 http://dx.doi.org/10.3389/fendo.2015.00159 Text en Copyright © 2015 Zhu and Zhou. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Zhu, Xiaoxia
Zhou, Wen
The Emerging Regulation of VEGFR-2 in Triple-Negative Breast Cancer
title The Emerging Regulation of VEGFR-2 in Triple-Negative Breast Cancer
title_full The Emerging Regulation of VEGFR-2 in Triple-Negative Breast Cancer
title_fullStr The Emerging Regulation of VEGFR-2 in Triple-Negative Breast Cancer
title_full_unstemmed The Emerging Regulation of VEGFR-2 in Triple-Negative Breast Cancer
title_short The Emerging Regulation of VEGFR-2 in Triple-Negative Breast Cancer
title_sort emerging regulation of vegfr-2 in triple-negative breast cancer
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598588/
https://www.ncbi.nlm.nih.gov/pubmed/26500608
http://dx.doi.org/10.3389/fendo.2015.00159
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