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Genome-wide Screens Implicate Loss of Cullin Ring Ligase 3 in Persistent Proliferation and Genome Instability in TP53 -Deficient Cells

Authors
  • Drainas, Alexandros P.1
  • Lambuta, Ruxandra A.1
  • Ivanova, Irina2
  • Serçin, Özdemirhan2
  • Sarropoulos, Ioannis1
  • Smith, Mike L.1
  • Efthymiopoulos, Theocharis1
  • Raeder, Benjamin1
  • Stütz, Adrian M.1
  • Waszak, Sebastian M.1
  • Mardin, Balca R.2
  • Korbel, Jan O.1
  • 1 European Molecular Biology Laboratory, Genome Biology Unit, Meyerhofstr. 1, 69117 Heidelberg, Germany
  • 2 BioMed X Innovation Center, 69120 Heidelberg, Germany
Type
Published Article
Journal
Cell Reports
Publisher
Elsevier
Publication Date
Apr 07, 2020
Volume
31
Issue
1
Identifiers
DOI: 10.1016/j.celrep.2020.03.029
PMID: 32268084
PMCID: PMC7166082
Source
PubMed Central
Keywords
License
Unknown

Abstract

Drainas et al. show that inactivation of genes in the neddylation pathway increases persistent proliferation in TP53 -deficient cells. TP53- and CUL3 -deficient cells induce an oncogenic transcriptional program, leading to partial EMT and heightened genomic instability. These cells show increased vulnerability to ATM inhibitors.

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