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

Navya Murugesan; Mayinuer Maitituoheti

doi:10.1080/23723556.2021.1984827

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

Navya Murugesan, Mayinuer Maitituoheti

Houston Methodist

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

Abstract

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.

Original language	English (US)
Article number	1984827
Journal	Molecular and Cellular Oncology
Volume	8
Issue number	5
DOIs	https://doi.org/10.1080/23723556.2021.1984827
State	Published - 2021

Keywords

KMT2D
enhancer reprogramming
glycolysis
melanoma

ASJC Scopus subject areas

Molecular Medicine
Cancer Research

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10.1080/23723556.2021.1984827

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title = " KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma",

abstract = "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.",

keywords = "KMT2D, enhancer reprogramming, glycolysis, melanoma",

author = "Navya Murugesan and Mayinuer Maitituoheti",

note = "Funding Information: This work was supported by the National Cancer Institute [CA222214]. Publisher Copyright: {\textcopyright} 2021 The Author(s). Published with license by Taylor \& Francis Group, LLC.",

year = "2021",

doi = "10.1080/23723556.2021.1984827",

language = "English (US)",

volume = "8",

journal = "Molecular and Cellular Oncology",

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T1 - KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma

AU - Murugesan, Navya

AU - Maitituoheti, Mayinuer

PY - 2021

Y1 - 2021

N2 - 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.

AB - 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.

KW - KMT2D

KW - enhancer reprogramming

KW - glycolysis

KW - melanoma

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JO - Molecular and Cellular Oncology

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M1 - 1984827

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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