FANCD2 limits replication stress and genome instability in cells lacking BRCA2

Nat Struct Mol Biol. 2016 Aug;23(8):755-757. doi: 10.1038/nsmb.3252. Epub 2016 Jun 20.


The tumor suppressor BRCA2 plays a key role in genome integrity by promoting replication-fork stability and homologous recombination (HR) DNA repair. Here we report that human cancer cells lacking BRCA2 rely on the Fanconi anemia protein FANCD2 to limit replication-fork progression and genomic instability. Our results identify a new role of FANCD2 in limiting constitutive replication stress in BRCA2-deficient cells, thereby affecting cell survival and treatment responses.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology
  • BRCA2 Protein / metabolism*
  • Cell Line, Tumor
  • Cell Survival
  • DNA Damage
  • DNA Replication
  • Fanconi Anemia Complementation Group D2 Protein / physiology*
  • Genome, Human
  • Genomic Instability
  • HEK293 Cells
  • Humans
  • Phthalazines / pharmacology
  • Piperazines / pharmacology


  • Antineoplastic Agents
  • BRCA2 Protein
  • BRCA2 protein, human
  • FANCD2 protein, human
  • Fanconi Anemia Complementation Group D2 Protein
  • Phthalazines
  • Piperazines
  • olaparib