Cancer-epigenetic function of the histone methyltransferase KMT2D and therapeutic opportunities for the treatment of KMT2D-deficient tumors

Shilpa S. Dhar; Min Gyu Lee

doi:10.18632/oncotarget.27988

Cancer-epigenetic function of the histone methyltransferase KMT2D and therapeutic opportunities for the treatment of KMT2D-deficient tumors

Shilpa S. Dhar, Min Gyu Lee

Molecular & Cellular Oncology

Research output: Contribution to journal › Review article › peer-review

19 Scopus citations

Abstract

Epigenetic mechanisms are central to understanding the molecular basis underlying tumorigenesis. Aberrations in epigenetic modifiers alter epigenomic landscapes and play a critical role in tumorigenesis. Notably, the histone lysine methyltransferase KMT2D (a COMPASS/ Set1 family member; also known as MLL4, ALR, and MLL2) is among the most frequently mutated genes in many different types of cancer. Recent studies have demonstrated how KMT2D loss induces abnormal epigenomic reprograming and rewires molecular pathways during tumorigenesis. These findings also have clinical and therapeutic implications for cancer treatment. In this review, we summarize recent advances in understanding the role of KMT2D in regulating tumorigenesis and discuss therapeutic opportunities for the treatment of KMT2D-deficient tumors.

Original language	English (US)
Pages (from-to)	1296-1308
Number of pages	13
Journal	Oncotarget
Volume	12
Issue number	13
DOIs	https://doi.org/10.18632/oncotarget.27988
State	Published - Jun 22 2021

Keywords

Cancer
Epigenetics
Histone methyltransferase
KMT2D
MLL4

ASJC Scopus subject areas

Oncology

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10.18632/oncotarget.27988

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title = "Cancer-epigenetic function of the histone methyltransferase KMT2D and therapeutic opportunities for the treatment of KMT2D-deficient tumors",

abstract = "Epigenetic mechanisms are central to understanding the molecular basis underlying tumorigenesis. Aberrations in epigenetic modifiers alter epigenomic landscapes and play a critical role in tumorigenesis. Notably, the histone lysine methyltransferase KMT2D (a COMPASS/ Set1 family member; also known as MLL4, ALR, and MLL2) is among the most frequently mutated genes in many different types of cancer. Recent studies have demonstrated how KMT2D loss induces abnormal epigenomic reprograming and rewires molecular pathways during tumorigenesis. These findings also have clinical and therapeutic implications for cancer treatment. In this review, we summarize recent advances in understanding the role of KMT2D in regulating tumorigenesis and discuss therapeutic opportunities for the treatment of KMT2D-deficient tumors.",

keywords = "Cancer, Epigenetics, Histone methyltransferase, KMT2D, MLL4",

author = "Dhar, {Shilpa S.} and Lee, {Min Gyu}",

note = "Funding Information: We thank Laura L. Russell, scientific editor, Research Medical Library in UT MD Anderson Cancer Center, for editing this article. This work was supported by grants to MG Lee from the National Institutes of Health (NIH): R01 CA207109 and R01 CA207098. Figures were created with https://biorender.com. We sincerely apologize for not citing and summarizing a number of relevant articles due to space limitation. Publisher Copyright: {\textcopyright} 2021 Impact Journals LLC. All rights reserved.",

year = "2021",

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AU - Dhar, Shilpa S.

AU - Lee, Min Gyu

N1 - Funding Information: We thank Laura L. Russell, scientific editor, Research Medical Library in UT MD Anderson Cancer Center, for editing this article. This work was supported by grants to MG Lee from the National Institutes of Health (NIH): R01 CA207109 and R01 CA207098. Figures were created with https://biorender.com. We sincerely apologize for not citing and summarizing a number of relevant articles due to space limitation. Publisher Copyright: © 2021 Impact Journals LLC. All rights reserved.

PY - 2021/6/22

Y1 - 2021/6/22

N2 - Epigenetic mechanisms are central to understanding the molecular basis underlying tumorigenesis. Aberrations in epigenetic modifiers alter epigenomic landscapes and play a critical role in tumorigenesis. Notably, the histone lysine methyltransferase KMT2D (a COMPASS/ Set1 family member; also known as MLL4, ALR, and MLL2) is among the most frequently mutated genes in many different types of cancer. Recent studies have demonstrated how KMT2D loss induces abnormal epigenomic reprograming and rewires molecular pathways during tumorigenesis. These findings also have clinical and therapeutic implications for cancer treatment. In this review, we summarize recent advances in understanding the role of KMT2D in regulating tumorigenesis and discuss therapeutic opportunities for the treatment of KMT2D-deficient tumors.

AB - Epigenetic mechanisms are central to understanding the molecular basis underlying tumorigenesis. Aberrations in epigenetic modifiers alter epigenomic landscapes and play a critical role in tumorigenesis. Notably, the histone lysine methyltransferase KMT2D (a COMPASS/ Set1 family member; also known as MLL4, ALR, and MLL2) is among the most frequently mutated genes in many different types of cancer. Recent studies have demonstrated how KMT2D loss induces abnormal epigenomic reprograming and rewires molecular pathways during tumorigenesis. These findings also have clinical and therapeutic implications for cancer treatment. In this review, we summarize recent advances in understanding the role of KMT2D in regulating tumorigenesis and discuss therapeutic opportunities for the treatment of KMT2D-deficient tumors.

KW - Cancer

KW - Epigenetics

KW - Histone methyltransferase

KW - KMT2D

KW - MLL4

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Cancer-epigenetic function of the histone methyltransferase KMT2D and therapeutic opportunities for the treatment of KMT2D-deficient tumors

Abstract

Keywords

ASJC Scopus subject areas

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