The USP7-TRIM27 axis mediates non-canonical PRC1.1 function and is a druggable target in leukemia.
Cancer
Cell Biology
Molecular Biology
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
21 May 2021
21 May 2021
Historique:
received:
25
11
2020
revised:
05
03
2021
accepted:
13
04
2021
entrez:
11
6
2021
pubmed:
12
6
2021
medline:
12
6
2021
Statut:
epublish
Résumé
In an attempt to unravel functionality of the non-canonical PRC1.1 Polycomb complex in human leukemogenesis, we show that USP7 and TRIM27 are integral components of PRC1.1. USP7 interactome analyses show that PRC1.1 is the predominant Polycomb complex co-precipitating with USP7. USP7 inhibition results in PRC1.1 disassembly and loss of chromatin binding, coinciding with reduced H2AK119ub and H3K27ac levels and diminished gene transcription of active PRC1.1-controlled loci, whereas H2AK119ub marks are also lost at PRC1 loci. TRIM27 and USP7 are reciprocally required for incorporation into PRC1.1, and TRIM27 knockdown partially rescues USP7 inhibitor sensitivity. USP7 inhibitors effectively impair proliferation in AML cells
Identifiants
pubmed: 34113809
doi: 10.1016/j.isci.2021.102435
pii: S2589-0042(21)00403-X
pmc: PMC8169803
doi:
Types de publication
Journal Article
Langues
eng
Pagination
102435Informations de copyright
© 2021 The Author(s).
Déclaration de conflit d'intérêts
The authors declare no conflict of interests.
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