DNA-PKcs promotes fork reversal and chemoresistance.


Journal

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

Informations de publication

Date de publication:
20 10 2022
Historique:
received: 08 03 2022
revised: 25 06 2022
accepted: 23 08 2022
pubmed: 22 9 2022
medline: 26 10 2022
entrez: 21 9 2022
Statut: ppublish

Résumé

The DNA-PKcs kinase mediates the repair of DNA double-strand breaks via classical non-homologous end joining (NHEJ). DNA-PKcs is also recruited to active replication forks, although a role for DNA-PKcs in the control of fork dynamics is unclear. Here, we identify a crucial role for DNA-PKcs in promoting fork reversal, a process that stabilizes stressed replication forks and protects genome integrity. DNA-PKcs promotes fork reversal and slowing in response to several replication stress-inducing agents in a manner independent of its role in NHEJ. Cells lacking DNA-PKcs activity show increased DNA damage during S-phase and cellular sensitivity to replication stress. Notably, prevention of fork slowing and reversal via DNA-PKcs inhibition efficiently restores chemotherapy sensitivity in BRCA2-deficient mammary tumors with acquired PARPi resistance. Together, our data uncover a new key regulator of fork reversal and show how DNA-PKcs signaling can be manipulated to alter fork dynamics and drug resistance in cancer.

Identifiants

pubmed: 36130596
pii: S1097-2765(22)00848-6
doi: 10.1016/j.molcel.2022.08.028
pmc: PMC9588680
mid: NIHMS1834570
pii:
doi:

Substances chimiques

DNA 9007-49-2

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

3932-3942.e6

Subventions

Organisme : NIGMS NIH HHS
ID : R01 GM097272
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM141159
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

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Auteurs

Diego Dibitetto (D)

Department of Molecular Biology and Genetics, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY 14853, USA; Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland. Electronic address: diego.dibitetto@vetsuisse.unibe.ch.

Shannon Marshall (S)

Department of Molecular Biology and Genetics, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY 14853, USA.

Andrea Sanchi (A)

Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland.

Martin Liptay (M)

Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland.

Jumana Badar (J)

Department of Molecular Biology and Genetics, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY 14853, USA.

Massimo Lopes (M)

Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland.

Sven Rottenberg (S)

Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland; Division of Molecular Pathology, the Netherlands Cancer Institute, 1066CX Amsterdam, the Netherlands; Bern Center for Precision Medicine, University of Bern, 3012 Bern, Switzerland.

Marcus B Smolka (MB)

Department of Molecular Biology and Genetics, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY 14853, USA. Electronic address: mbs266@cornell.edu.

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Classifications MeSH