KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma

We reported that histone H3 lysine (K) 4 methyltransferase, KMT2D, serves as a potent tumor-suppressor in melanoma, which was identified via in vivo epigenome-focused RNA interference (RNAi) screen. KMT2D-deficient tumors show substantial reprogramming of key metabolic pathways including glycolysis...

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Autores principales: Murugesan, Navya, Maitituoheti, Mayinuer
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Author’s Views
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8632269/
https://www.ncbi.nlm.nih.gov/pubmed/34859145
http://dx.doi.org/10.1080/23723556.2021.1984827
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author Murugesan, Navya
Maitituoheti, Mayinuer
author_facet Murugesan, Navya
Maitituoheti, Mayinuer
author_sort Murugesan, Navya
collection PubMed
description We reported that histone H3 lysine (K) 4 methyltransferase, KMT2D, serves as a potent tumor-suppressor in melanoma, which was identified via in vivo epigenome-focused RNA interference (RNAi) screen. KMT2D-deficient tumors show substantial reprogramming of key metabolic pathways including glycolysis via reduction of H3K4me1 (Histone H3K4 mono-methylation)-marked active enhancers, conferring sensitivity to inhibitors of glycolysis and IGFR (Insulin Growth Factor Receptor) pathway.
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spelling pubmed-86322692021-12-01 KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma Murugesan, Navya Maitituoheti, Mayinuer Mol Cell Oncol Author’s Views We reported that histone H3 lysine (K) 4 methyltransferase, KMT2D, serves as a potent tumor-suppressor in melanoma, which was identified via in vivo epigenome-focused RNA interference (RNAi) screen. KMT2D-deficient tumors show substantial reprogramming of key metabolic pathways including glycolysis via reduction of H3K4me1 (Histone H3K4 mono-methylation)-marked active enhancers, conferring sensitivity to inhibitors of glycolysis and IGFR (Insulin Growth Factor Receptor) pathway. Taylor & Francis 2021-11-01 /pmc/articles/PMC8632269/ /pubmed/34859145 http://dx.doi.org/10.1080/23723556.2021.1984827 Text en © 2021 The Author(s). Published with license by Taylor & Francis Group, LLC. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.
spellingShingle Author’s Views
Murugesan, Navya
Maitituoheti, Mayinuer
KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma
title KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma
title_full KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma
title_fullStr KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma
title_full_unstemmed KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma
title_short KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma
title_sort kmt2d deficiency confers a therapeutic vulnerability to glycolytic and igfr inhibitors in melanoma
topic Author’s Views
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8632269/
https://www.ncbi.nlm.nih.gov/pubmed/34859145
http://dx.doi.org/10.1080/23723556.2021.1984827
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