The Oncogenic Helicase ALC1 Regulates PARP Inhibitor Potency by Trapping PARP2 at DNA Breaks.


Journal

Molecular cell
ISSN: 1097-4164
Titre abrégé: Mol Cell
Pays: United States
ID NLM: 9802571

Informations de publication

Date de publication:
03 12 2020
Historique:
received: 13 05 2020
revised: 27 08 2020
accepted: 04 10 2020
entrez: 4 12 2020
pubmed: 5 12 2020
medline: 17 12 2020
Statut: ppublish

Résumé

The anti-tumor potency of poly(ADP-ribose) polymerase (PARP) inhibitors (PARPis) has been linked to trapping of PARP1 on damaged chromatin. However, little is known about their impact on PARP2, an isoform with overlapping functions at DNA lesions. Whether the release of PARP1/2 from DNA lesions is actively catalyzed by molecular machines is also not known. We found that PARPis robustly trap PARP2 and that the helicase ALC1 (CHD1L) is strictly required for PARP2 release. Catalytic inactivation of ALC1 quantitatively traps PARP2 but not PARP1. ALC1 manipulation impacts the response to single-strand DNA breaks through PARP2 trapping, potentiates PARPi-induced cancer cell killing, and mediates synthetic lethality upon BRCA deficiency. The chromatin remodeler ALC1 actively drives PARP2 turnover from DNA lesions, and PARP2 contributes to the cellular responses of PARPi. This suggests that disrupting the ATP-fueled remodeling forces of ALC1 might enable therapies that selectively target the DNA repair functions of PARPs in cancer.

Identifiants

pubmed: 33275888
pii: S1097-2765(20)30692-4
doi: 10.1016/j.molcel.2020.10.009
pii:
doi:

Substances chimiques

DNA-Binding Proteins 0
Poly(ADP-ribose) Polymerase Inhibitors 0
Proto-Oncogene Proteins 0
PARP1 protein, human EC 2.4.2.30
PARP2 protein, human EC 2.4.2.30
Poly (ADP-Ribose) Polymerase-1 EC 2.4.2.30
Poly(ADP-ribose) Polymerases EC 2.4.2.30
DNA Helicases EC 3.6.4.-
CHD1L protein, human EC 3.6.4.12

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

862-875.e6

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Interests A.S. and A.G.L. are co-founders and shareholders of Eisbach Bio, a biotech developing small-molecule inhibitors targeting helicases.

Auteurs

Charlotte Blessing (C)

Department of Physiological Chemistry, Biomedical Center (BMC), Faculty of Medicine, LMU Munich, 82152 Planegg-Martinsried, Germany; International Max Planck Research School (IMPRS) for Molecular Life Sciences, 82152 Planegg-Martinsried, Germany.

Imke Karlijn Mandemaker (IK)

Department of Physiological Chemistry, Biomedical Center (BMC), Faculty of Medicine, LMU Munich, 82152 Planegg-Martinsried, Germany.

Claudia Gonzalez-Leal (C)

Department of Physiological Chemistry, Biomedical Center (BMC), Faculty of Medicine, LMU Munich, 82152 Planegg-Martinsried, Germany; International Max Planck Research School (IMPRS) for Molecular Life Sciences, 82152 Planegg-Martinsried, Germany.

Julia Preisser (J)

Department of Physiological Chemistry, Biomedical Center (BMC), Faculty of Medicine, LMU Munich, 82152 Planegg-Martinsried, Germany.

Adrian Schomburg (A)

Department of Physiological Chemistry, Biomedical Center (BMC), Faculty of Medicine, LMU Munich, 82152 Planegg-Martinsried, Germany; Eisbach Bio GmbH, Am Klopferspitz 19, 82152 Planegg-Martinsried, Germany.

Andreas Gerhard Ladurner (AG)

Department of Physiological Chemistry, Biomedical Center (BMC), Faculty of Medicine, LMU Munich, 82152 Planegg-Martinsried, Germany; International Max Planck Research School (IMPRS) for Molecular Life Sciences, 82152 Planegg-Martinsried, Germany; Eisbach Bio GmbH, Am Klopferspitz 19, 82152 Planegg-Martinsried, Germany. Electronic address: andreas.ladurner@bmc.med.lmu.de.

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Classifications MeSH