Trabectedin Inhibits EWS-FLI1 and Evicts SWI/SNF from Chromatin in a Schedule-dependent Manner.


Journal

Clinical cancer research : an official journal of the American Association for Cancer Research
ISSN: 1557-3265
Titre abrégé: Clin Cancer Res
Pays: United States
ID NLM: 9502500

Informations de publication

Date de publication:
01 06 2019
Historique:
received: 26 10 2018
revised: 24 12 2018
accepted: 23 01 2019
pubmed: 7 2 2019
medline: 7 7 2020
entrez: 7 2 2019
Statut: ppublish

Résumé

The successful clinical translation of compounds that target specific oncogenic transcription factors will require an understanding of the mechanism of target suppression to optimize the dose and schedule of administration. We have previously shown trabectedin reverses the gene signature of the EWS-FLI1 transcription factor. In this report, we establish the mechanism of suppression and use it to justify the reevaluation of this drug in the clinic in patients with Ewing sarcoma. Trabectedin evicts the SWI/SNF chromatin-remodeling complex from chromatin and redistributes EWS-FLI1 in the nucleus leading to a marked increase in H3K27me3 and H3K9me3 at EWS-FLI1 target genes. These effects only occur at high concentrations of trabectedin leading to suppression of EWS-FLI1 target genes and a loss of cell viability. These data provide the justification to evaluate trabectedin in the clinic on a short infusion schedule in combination with low-dose irinotecan with

Identifiants

pubmed: 30723142
pii: 1078-0432.CCR-18-3511
doi: 10.1158/1078-0432.CCR-18-3511
pmc: PMC6594545
mid: NIHMS1520011
doi:

Substances chimiques

Antineoplastic Agents, Alkylating 0
Chromatin 0
EWS-FLI fusion protein 0
Oncogene Proteins, Fusion 0
Proto-Oncogene Protein c-fli-1 0
RNA-Binding Protein EWS 0
Transcription Factors 0
Trabectedin ID0YZQ2TCP

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

3417-3429

Subventions

Organisme : NCI NIH HHS
ID : R01 CA188314
Pays : United States
Organisme : NCI NIH HHS
ID : F31 CA236300
Pays : United States
Organisme : NCI NIH HHS
ID : U54 CA231641
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA183776
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM124736
Pays : United States

Informations de copyright

©2019 American Association for Cancer Research.

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Auteurs

Matt L Harlow (ML)

Department of Cancer Biology, Vanderbilt University, Nashville, Tennessee.

Maggie H Chasse (MH)

Van Andel Research Institute, Grand Rapids, Michigan.

Elissa A Boguslawski (EA)

Van Andel Research Institute, Grand Rapids, Michigan.

Katie M Sorensen (KM)

Van Andel Research Institute, Grand Rapids, Michigan.

Jenna M Gedminas (JM)

Van Andel Research Institute, Grand Rapids, Michigan.
Department of Pediatrics, Michigan State University, East Lansing, Michigan.
Division of Pediatric Hematology/Oncology, Helen DeVos Children's Hospital, Grand Rapids, Michigan.

Susan M Kitchen-Goosen (SM)

Van Andel Research Institute, Grand Rapids, Michigan.

Scott B Rothbart (SB)

Van Andel Research Institute, Grand Rapids, Michigan.

Cenny Taslim (C)

Center for Childhood Cancer and Blood Diseases, Nationwide Children's Hospital Research Institute, Columbus, Ohio.

Stephen L Lessnick (SL)

Center for Childhood Cancer and Blood Diseases, Nationwide Children's Hospital Research Institute, Columbus, Ohio.
Division of Pediatric Hematology/Oncology/BMT, The Ohio State University College of Medicine, Columbus, Ohio.

Anderson S Peck (AS)

Van Andel Research Institute, Grand Rapids, Michigan.

Zachary B Madaj (ZB)

Van Andel Research Institute, Grand Rapids, Michigan.

Megan J Bowman (MJ)

Van Andel Research Institute, Grand Rapids, Michigan.

Patrick J Grohar (PJ)

Van Andel Research Institute, Grand Rapids, Michigan. Patrick.grohar@vai.org.
Department of Pediatrics, Michigan State University, East Lansing, Michigan.
Division of Pediatric Hematology/Oncology, Helen DeVos Children's Hospital, Grand Rapids, Michigan.

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