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

Shilpa S. Dhar and Min Gyu Lee _

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Oncotarget. 2021; 12:1296-1308. https://doi.org/10.18632/oncotarget.27988

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Abstract

Shilpa S. Dhar1 and Min Gyu Lee1,2

1 Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA

2 The Center for Cancer Epigenetics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA

Correspondence to:

Min Gyu Lee,email: mglee@mdanderson.org

Keywords: cancer; epigenetics; histone methyltransferase; KMT2D; MLL4

Received: May 27, 2021     Accepted: June 01, 2021     Published: June 22, 2021

Copyright: © 2021 Dhar and Lee. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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.


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