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Hypoxia and Inflammation in Cancer, Focus on HIF and NF-κB

Cancer is often characterised by the presence of hypoxia and inflammation. Paramount to the mechanisms controlling cellular responses under such stress stimuli, are the transcription factor families of Hypoxia Inducible Factor (HIF) and Nuclear Factor of κ-light-chain-enhancer of activated B cells (...

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Autores principales: D’Ignazio, Laura, Batie, Michael, Rocha, Sonia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5489807/
https://www.ncbi.nlm.nih.gov/pubmed/28536364
http://dx.doi.org/10.3390/biomedicines5020021
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author D’Ignazio, Laura
Batie, Michael
Rocha, Sonia
author_facet D’Ignazio, Laura
Batie, Michael
Rocha, Sonia
author_sort D’Ignazio, Laura
collection PubMed
description Cancer is often characterised by the presence of hypoxia and inflammation. Paramount to the mechanisms controlling cellular responses under such stress stimuli, are the transcription factor families of Hypoxia Inducible Factor (HIF) and Nuclear Factor of κ-light-chain-enhancer of activated B cells (NF-κB). Although, a detailed understating of how these transcription factors respond to their cognate stimulus is well established, it is now appreciated that HIF and NF-κB undergo extensive crosstalk, in particular in pathological situations such as cancer. Here, we focus on the current knowledge on how HIF is activated by inflammation and how NF-κB is modulated by hypoxia. We summarise the evidence for the possible mechanism behind this activation and how HIF and NF-κB function impacts cancer, focusing on colorectal, breast and lung cancer. We discuss possible new points of therapeutic intervention aiming to harness the current understanding of the HIF-NF-κB crosstalk.
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spelling pubmed-54898072017-06-30 Hypoxia and Inflammation in Cancer, Focus on HIF and NF-κB D’Ignazio, Laura Batie, Michael Rocha, Sonia Biomedicines Review Cancer is often characterised by the presence of hypoxia and inflammation. Paramount to the mechanisms controlling cellular responses under such stress stimuli, are the transcription factor families of Hypoxia Inducible Factor (HIF) and Nuclear Factor of κ-light-chain-enhancer of activated B cells (NF-κB). Although, a detailed understating of how these transcription factors respond to their cognate stimulus is well established, it is now appreciated that HIF and NF-κB undergo extensive crosstalk, in particular in pathological situations such as cancer. Here, we focus on the current knowledge on how HIF is activated by inflammation and how NF-κB is modulated by hypoxia. We summarise the evidence for the possible mechanism behind this activation and how HIF and NF-κB function impacts cancer, focusing on colorectal, breast and lung cancer. We discuss possible new points of therapeutic intervention aiming to harness the current understanding of the HIF-NF-κB crosstalk. MDPI 2017-05-09 /pmc/articles/PMC5489807/ /pubmed/28536364 http://dx.doi.org/10.3390/biomedicines5020021 Text en © 2017 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 (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
D’Ignazio, Laura
Batie, Michael
Rocha, Sonia
Hypoxia and Inflammation in Cancer, Focus on HIF and NF-κB
title Hypoxia and Inflammation in Cancer, Focus on HIF and NF-κB
title_full Hypoxia and Inflammation in Cancer, Focus on HIF and NF-κB
title_fullStr Hypoxia and Inflammation in Cancer, Focus on HIF and NF-κB
title_full_unstemmed Hypoxia and Inflammation in Cancer, Focus on HIF and NF-κB
title_short Hypoxia and Inflammation in Cancer, Focus on HIF and NF-κB
title_sort hypoxia and inflammation in cancer, focus on hif and nf-κb
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5489807/
https://www.ncbi.nlm.nih.gov/pubmed/28536364
http://dx.doi.org/10.3390/biomedicines5020021
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