Novel insights into histone lysine methyltransferases in cancer therapy: From epigenetic regulation to selective drugs

被引：19

作者：

Liao, Qili ^{[1
,2
]}

Yang, Jie ^{[1
,2
]}

Ge, Shengfang ^{[1
,2
]}

Chai, Peiwei ^{[1
,2
]}

Fan, Jiayan ^{[1
,2
]}

Jia, Renbing ^{[1
,2
]}

机构：

[1] Shanghai Jiao Tong Univ, Peoples Hosp 9, Dept Ophthalmol, Sch Med, Shanghai 200001, Peoples R China

[2] Shanghai Key Lab Orbital Dis & Ocular Oncol, Shanghai 200001, Peoples R China

来源：

JOURNAL OF PHARMACEUTICAL ANALYSIS | 2023年 / 13卷 / 02期

基金：

中国国家自然科学基金;

关键词：

Cancer; Epigenetics; Histone lysine methyltransferase; Epigenetic inhibitors; Combined therapeutic strategy; Clinical application; TYROSINE KINASE INHIBITORS; SMALL-MOLECULE INHIBITOR; MLL-REARRANGED LEUKEMIA; CELL LUNG-CANCER; GENE-EXPRESSION; H3K79; METHYLATION; GASTRIC-CANCER; CHEMICAL PROBE; SINGLE-ARM; OPEN-LABEL;

D O I：

10.1016/j.jpha.2022.11.009

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

The reversible and precise temporal and spatial regulation of histone lysine methyltransferases (KMTs) is essential for epigenome homeostasis. The dysregulation of KMTs is associated with tumor initiation, metastasis, chemoresistance, invasiveness, and the immune microenvironment. Therapeutically, their promising effects are being evaluated in diversified preclinical and clinical trials, demonstrating encouraging outcomes in multiple malignancies. In this review, we have updated recent understandings of KMTs' functions and the development of their targeted inhibitors. First, we provide an updated overview of the regulatory roles of several KMT activities in oncogenesis, tumor suppression, and im-mune regulation. In addition, we summarize the current targeting strategies in different cancer types and multiple ongoing clinical trials of combination therapies with KMT inhibitors. In summary, we endeavor to depict the regulation of KMT-mediated epigenetic landscape and provide potential epigenetic targets in the treatment of cancers.(c) 2022 Published by Elsevier B.V. on behalf of Xi'an Jiaotong University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

引用

页码：127 / 141

页数：15

共 152 条

[11] DOT1L-controlled cell-fate determination and transcription elongation are independent of H3K79 methylation [J].

Cao, Kaixiang ;

Ugarenko, Michal ;

Ozark, Patrick A. ;

Wang, Juan ;

Marshall, Stacy A. ;

Rendleman, Emily J. ;

Liang, Kaiwei ;

Wang, Lu ;

Zou, Lihua ;

Smith, Edwin R. ;

Yue, Feng ;

Shilatifard, Ali .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2020, 117 (44) :27365-27373

[12] Combined Inhibition of G9a and EZH2 Suppresses Tumor Growth via Synergistic Induction of IL24-Mediated Apoptosis [J].

Casciello, Francesco ;

Kelly, Gregory M. ;

Ramarao-Milne, Priya ;

Kamal, Nabilah ;

Stewart, Teneale A. ;

Mukhopadhyay, Pamela ;

Kazakoff, Stephen H. ;

Miranda, Mariska ;

Kim, Dorim ;

Davis, Felicity M. ;

Hayward, Nicholas K. ;

Vertino, Paula M. ;

Waddell, Nicola ;

Gannon, Frank ;

Lee, Jason S. .

CANCER RESEARCH, 2022, 82 (06) :1208-1221

[13] Regulation of epigenetic homeostasis in uveal melanoma and retinoblastoma [J].

Chai, Peiwei ;

Jia, Ruobing ;

Li, Yongyun ;

Zhou, Chuandi ;

Gu, Xiang ;

Yang, Ludi ;

Shi, Hanhan ;

Tian, Hao ;

Lin, Huimin ;

Yu, Jie ;

Zhuang, Ai ;

Ge, Shengfang ;

Jia, Renbing ;

Fan, Xianqun .

PROGRESS IN RETINAL AND EYE RESEARCH, 2022, 89

[14] Disruptor of telomeric silencing 1-like promotes ovarian cancer tumor growth by stimulating pro-tumorigenic metabolic pathways and blocking apoptosis [J].

Chava, Suresh ;

Bugide, Suresh ;

Edwards, Yvonne J. K. ;

Gupta, Romi .

ONCOGENESIS, 2021, 10 (07)

[15] DOT1L inhibits SIRT1-mediated epigenetic silencing to maintain leukemic gene expression in MLL-rearranged leukemia [J].

Chen, Chun-Wei ;

Koche, Richard P. ;

Sinha, Amit U. ;

Deshpande, Aniruddha J. ;

Zhu, Nan ;

Eng, Rowena ;

Doench, John G. ;

Xu, Haiming ;

Chu, Scott H. ;

Qi, Jun ;

Wang, Xi ;

Delaney, Christopher ;

Bernt, Kathrin M. ;

Root, David E. ;

Hahn, William C. ;

Bradner, James E. ;

Armstrong, Scott A. .

NATURE MEDICINE, 2015, 21 (04) :335-+

[16] Complementary activities of DOT1L and Menin inhibitors in MLL-rearranged leukemia [J].

Dafflon, C. ;

Craig, V. J. ;

Mereau, H. ;

Graesel, J. ;

Engstler, B. Schacher ;

Hoffman, G. ;

Nigsch, F. ;

Gaulis, S. ;

Barys, L. ;

Ito, M. ;

Aguade-Gorgorio, J. ;

Bornhauser, B. ;

Bourquin, J-P ;

Proske, A. ;

Stork-Fux, C. ;

Murakami, M. ;

Sellers, W. R. ;

Hofmann, F. ;

Schwaller, J. ;

Tiedt, R. .

LEUKEMIA, 2017, 31 (06) :1269-1277

[17] Potent inhibition of DOT1L as treatment of MLL-fusion leukemia [J].

Daigle, Scott R. ;

Olhava, Edward J. ;

Therkelsen, Carly A. ;

Basavapathruni, Aravind ;

Jin, Lei ;

Boriack-Sjodin, P. Ann ;

Allain, Christina J. ;

Klaus, Christine R. ;

Raimondi, Alejandra ;

Scott, Margaret Porter ;

Waters, Nigel J. ;

Chesworth, Richard ;

Moyer, Mikel P. ;

Copeland, Robert A. ;

Richon, Victoria M. ;

Pollock, Roy M. .

BLOOD, 2013, 122 (06) :1017-1025

[18] Selective Killing of Mixed Lineage Leukemia Cells by a Potent Small-Molecule DOT1L Inhibitor [J].

Daigle, Scott R. ;

Olhava, Edward J. ;

Therkelsen, Carly A. ;

Majer, Christina R. ;

Sneeringer, Christopher J. ;

Song, Jeffrey ;

Johnston, L. Danielle ;

Scott, Margaret Porter ;

Smith, Jesse J. ;

Xiao, Yonghong ;

Jin, Lei ;

Kuntz, Kevin W. ;

Chesworth, Richard ;

Moyer, Mike P. ;

Bernt, Kathrin M. ;

Tseng, Jen-Chieh ;

Kung, Andrew L. ;

Armstrong, Scott A. ;

Copeland, Robert A. ;

Richon, Victoria M. ;

Pollock, Roy M. .

CANCER CELL, 2011, 20 (01) :53-65

[19] Advancing targeted protein degradation for cancer therapy [J].

Dale, Brandon ;

Cheng, Meng ;

Park, Kwang-Su ;

Kaniskan, H. Umit ;

Xiong, Yue ;

Jin, Jian .

NATURE REVIEWS CANCER, 2021, 21 (10) :638-654

[20] Cancer Epigenetics: From Mechanism to Therapy [J].

Dawson, Mark A. ;

Kouzarides, Tony .

CELL, 2012, 150 (01) :12-27

← 1 2 3 4 5 6 7 8 9 10 →