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EPAS-1 Mediates SP-1-Dependent FBI-1 Expression and Regulates Tumor Cell Survival and Proliferation

Factor binding IST-1 (FBI-1) plays an important role in oncogenic transformation and tumorigenesis. As FBI-1 is over-expressed in multiple human cancers, the regulation of itself would provide new effective options for cancer intervention. In this work, we aimed to study the role that EPAS-1 plays i...

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Detalles Bibliográficos
Autores principales: Wang, Xiaogang, Cao, Peng, Li, Zhiqing, Wu, Dongyang, Wang, Xi, Liang, Guobiao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200855/
https://www.ncbi.nlm.nih.gov/pubmed/25192290
http://dx.doi.org/10.3390/ijms150915689
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author Wang, Xiaogang
Cao, Peng
Li, Zhiqing
Wu, Dongyang
Wang, Xi
Liang, Guobiao
author_facet Wang, Xiaogang
Cao, Peng
Li, Zhiqing
Wu, Dongyang
Wang, Xi
Liang, Guobiao
author_sort Wang, Xiaogang
collection PubMed
description Factor binding IST-1 (FBI-1) plays an important role in oncogenic transformation and tumorigenesis. As FBI-1 is over-expressed in multiple human cancers, the regulation of itself would provide new effective options for cancer intervention. In this work, we aimed to study the role that EPAS-1 plays in regulating FBI-1. We use the fact that specificity protein-1 (SP-1) is one of the crucial transcription factors of FBI-1, and that SP-1 can interact with the endothelial pas domain protein-1 (EPAS-1) for the induction of hypoxia related genes. The study showed that EPAS-1 plays an indispensible role in SP-1 transcription factor-mediated FBI-1 induction, and participated in tumor cell survival and proliferation. Thus, EPAS-1 could be a novel target for cancer therapeutics.
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spelling pubmed-42008552014-10-17 EPAS-1 Mediates SP-1-Dependent FBI-1 Expression and Regulates Tumor Cell Survival and Proliferation Wang, Xiaogang Cao, Peng Li, Zhiqing Wu, Dongyang Wang, Xi Liang, Guobiao Int J Mol Sci Article Factor binding IST-1 (FBI-1) plays an important role in oncogenic transformation and tumorigenesis. As FBI-1 is over-expressed in multiple human cancers, the regulation of itself would provide new effective options for cancer intervention. In this work, we aimed to study the role that EPAS-1 plays in regulating FBI-1. We use the fact that specificity protein-1 (SP-1) is one of the crucial transcription factors of FBI-1, and that SP-1 can interact with the endothelial pas domain protein-1 (EPAS-1) for the induction of hypoxia related genes. The study showed that EPAS-1 plays an indispensible role in SP-1 transcription factor-mediated FBI-1 induction, and participated in tumor cell survival and proliferation. Thus, EPAS-1 could be a novel target for cancer therapeutics. MDPI 2014-09-04 /pmc/articles/PMC4200855/ /pubmed/25192290 http://dx.doi.org/10.3390/ijms150915689 Text en © 2014 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Article
Wang, Xiaogang
Cao, Peng
Li, Zhiqing
Wu, Dongyang
Wang, Xi
Liang, Guobiao
EPAS-1 Mediates SP-1-Dependent FBI-1 Expression and Regulates Tumor Cell Survival and Proliferation
title EPAS-1 Mediates SP-1-Dependent FBI-1 Expression and Regulates Tumor Cell Survival and Proliferation
title_full EPAS-1 Mediates SP-1-Dependent FBI-1 Expression and Regulates Tumor Cell Survival and Proliferation
title_fullStr EPAS-1 Mediates SP-1-Dependent FBI-1 Expression and Regulates Tumor Cell Survival and Proliferation
title_full_unstemmed EPAS-1 Mediates SP-1-Dependent FBI-1 Expression and Regulates Tumor Cell Survival and Proliferation
title_short EPAS-1 Mediates SP-1-Dependent FBI-1 Expression and Regulates Tumor Cell Survival and Proliferation
title_sort epas-1 mediates sp-1-dependent fbi-1 expression and regulates tumor cell survival and proliferation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200855/
https://www.ncbi.nlm.nih.gov/pubmed/25192290
http://dx.doi.org/10.3390/ijms150915689
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