Therapeutic Targeting of EZH2 and BET BRD4 in Pediatric Rhabdoid Tumors.


Journal

Molecular cancer therapeutics
ISSN: 1538-8514
Titre abrégé: Mol Cancer Ther
Pays: United States
ID NLM: 101132535

Informations de publication

Date de publication:
04 05 2022
Historique:
received: 28 07 2021
revised: 20 12 2021
accepted: 10 02 2022
pubmed: 6 3 2022
medline: 6 5 2022
entrez: 5 3 2022
Statut: ppublish

Résumé

Aberrant activity of the H3K27 modifiers EZH2 and BRD4 is an important oncogenic driver for atypical teratoid/rhabdoid tumor (AT/RT), and each is potentially a possible therapeutic target for treating AT/RT. We, therefore, determined whether targeting distinct histone modifier activities was an effective approach for treating AT/RT. The effects of EZH2 and BRD4 inhibition on histone modification, cell proliferation, and cell invasion were analyzed by immunoblotting, MTS assay, colony formation assay, and cell invasion assay. RNA- and chromatin immunoprecipitation-sequencing were used to determine transcriptional and epigenetic changes in AT/RT cells treated with EZH2 and BRD4 inhibitors. We treated mice bearing human AT/RT xenografts with EZH2 and BRD4 inhibitors. Intracranial tumor growth was monitored by bioluminescence imaging, and the therapeutic response was evaluated by animal survival. AT/RT cells showed elevated levels of H3K27 trimethylation (H3K27me3) and H3K27 acetylation (H3K27ac), with expression of EZH2 and BRD4, and lack of SMARCB1 proteins. Targeted inhibition of EZH2 and BRD4 activities reduced cell proliferation and invasiveness of AT/RT in association with decreasing H3K27me3 and H3K27ac. Differential genomic occupancy of H3K27me3 and H3K27ac regulated specific gene expression in response to EZH2 and BRD4 inhibitions. A combination of EZH2 and BRD4 inhibition increased the therapeutic benefit in vitro and in vivo, outperforming either monotherapy. Overall, histones H3K27me3 and H3K27ac were elevated in AT/RT cells and distributed in distinct chromatin regions to regulate specific gene expression and to promote AT/RT growth. Targeting EZH2 and BRD4 activity is, therefore, a potential combination therapy for AT/RT.

Identifiants

pubmed: 35247919
pii: 681957
doi: 10.1158/1535-7163.MCT-21-0646
pmc: PMC9081147
mid: NIHMS1783719
doi:

Substances chimiques

BRD4 protein, human 0
Cell Cycle Proteins 0
Histones 0
Nuclear Proteins 0
Transcription Factors 0
EZH2 protein, human EC 2.1.1.43
Enhancer of Zeste Homolog 2 Protein EC 2.1.1.43

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

715-726

Subventions

Organisme : NCI NIH HHS
ID : K99 CA234434
Pays : United States
Organisme : NCI NIH HHS
ID : R35 CA197569
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS093079
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS126513
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA214035
Pays : United States
Organisme : NIAMS NIH HHS
ID : P30 AR075049
Pays : United States

Informations de copyright

©2022 American Association for Cancer Research.

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Auteurs

Yukitomo Ishi (Y)

Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Yongzhan Zhang (Y)

Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Department of Biology, Institute of Molecular Health Sciences, ETH Zürich, Zürich, Switzerland.

Ali Zhang (A)

Department of Neurosurgical Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Takahiro Sasaki (T)

Department of Neurosurgical Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Andrea Piunti (A)

Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Amreena Suri (A)

Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Jun Watanabe (J)

Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Department of Neurological Surgery, Brain Research Institute, Niigata University, Niigata, Japan.

Kouki Abe (K)

Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Xingyao He (X)

Department of Neurosurgical Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Hiroaki Katagi (H)

Department of Neurosurgical Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Pankaj Bhalla (P)

Department of Dermatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Manabu Natsumeda (M)

Department of Neurological Surgery, Brain Research Institute, Niigata University, Niigata, Japan.

Lihua Zou (L)

Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Ali Shilatifard (A)

Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Rintaro Hashizume (R)

Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Neuro-Oncology and Stem Cells Transplantation, Ann and Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois.

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