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Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer

Non-small cell lung cancer (NSCLC) has been the leading cause of cancer-related death worldwide, over the last few decades. Survival remains extremely poor in the metastatic setting and, consequently, innovative therapeutic strategies are urgently needed. Inhibitor of Growth Gene 2 (ING2) is a core...

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Detalles Bibliográficos
Autores principales: Blondel, Alice, Benberghout, Amine, Pedeux, Rémy, Ricordel, Charles
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6827349/
https://www.ncbi.nlm.nih.gov/pubmed/31640185
http://dx.doi.org/10.3390/cancers11101601
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author Blondel, Alice
Benberghout, Amine
Pedeux, Rémy
Ricordel, Charles
author_facet Blondel, Alice
Benberghout, Amine
Pedeux, Rémy
Ricordel, Charles
author_sort Blondel, Alice
collection PubMed
description Non-small cell lung cancer (NSCLC) has been the leading cause of cancer-related death worldwide, over the last few decades. Survival remains extremely poor in the metastatic setting and, consequently, innovative therapeutic strategies are urgently needed. Inhibitor of Growth Gene 2 (ING2) is a core component of the mSin3A/Histone deacetylases complex (HDAC), which controls the chromatin acetylation status and modulates gene transcription. This gene has been characterized as a tumor suppressor gene and its status in cancer has been scarcely explored. In this review, we focused on ING2 and other mSin3A/HDAC member statuses in NSCLC. Taking advantage of existing public databases and known pharmacological properties of HDAC inhibitors, finally, we proposed a therapeutic model based on an ING2 biomarker-guided strategy.
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spelling pubmed-68273492019-11-18 Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer Blondel, Alice Benberghout, Amine Pedeux, Rémy Ricordel, Charles Cancers (Basel) Review Non-small cell lung cancer (NSCLC) has been the leading cause of cancer-related death worldwide, over the last few decades. Survival remains extremely poor in the metastatic setting and, consequently, innovative therapeutic strategies are urgently needed. Inhibitor of Growth Gene 2 (ING2) is a core component of the mSin3A/Histone deacetylases complex (HDAC), which controls the chromatin acetylation status and modulates gene transcription. This gene has been characterized as a tumor suppressor gene and its status in cancer has been scarcely explored. In this review, we focused on ING2 and other mSin3A/HDAC member statuses in NSCLC. Taking advantage of existing public databases and known pharmacological properties of HDAC inhibitors, finally, we proposed a therapeutic model based on an ING2 biomarker-guided strategy. MDPI 2019-10-21 /pmc/articles/PMC6827349/ /pubmed/31640185 http://dx.doi.org/10.3390/cancers11101601 Text en © 2019 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
Blondel, Alice
Benberghout, Amine
Pedeux, Rémy
Ricordel, Charles
Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer
title Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer
title_full Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer
title_fullStr Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer
title_full_unstemmed Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer
title_short Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer
title_sort exploiting ing2 epigenetic modulation as a therapeutic opportunity for non-small cell lung cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6827349/
https://www.ncbi.nlm.nih.gov/pubmed/31640185
http://dx.doi.org/10.3390/cancers11101601
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