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53BP1 loss rescues BRCA1 deficiency and is associated with triple-negative and BRCA-mutated breast cancers

P Bouwman, A Aly, JM Escandell, M Pieterse, J Bartkova, der Gulden H van, S Hiddingh, M Thanasoula, A Kulkarni, Q Yang, BG Haffty, J Tommiska, C Blomqvist, R Drapkin, DJ Adams, H Nevanlinna, J Bartek, M Tarsounas, S Ganesan, J Jonkers

. 2010 ; 17 (6) : 688-695.

Jazyk angličtina Země Spojené státy americké

Perzistentní odkaz   https://www.medvik.cz/link/bmc14075888
E-zdroje Online Plný text

NLK ProQuest Central od 1997-02-01 do Před 1 rokem
Medline Complete (EBSCOhost) od 2004-01-01 do 2015-11-30
Health & Medicine (ProQuest) od 1997-02-01 do Před 1 rokem

Odkazy

PubMed 20453858
DOI 10.1038/nsmb.1831
Knihovny.cz E-zdroje

Germ-line mutations in breast cancer 1, early onset (BRCA1) result in predisposition to breast and ovarian cancer. BRCA1-mutated tumors show genomic instability, mainly as a consequence of impaired recombinatorial DNA repair. Here we identify p53-binding protein 1 (53BP1) as an essential factor for sustaining the growth arrest induced by Brca1 deletion. Depletion of 53BP1 abrogates the ATM-dependent checkpoint response and G2 cell-cycle arrest triggered by the accumulation of DNA breaks in Brca1-deleted cells. This effect of 53BP1 is specific to BRCA1 function, as 53BP1 depletion did not alleviate proliferation arrest or checkpoint responses in Brca2-deleted cells. Notably, loss of 53BP1 partially restores the homologous-recombination defect of Brca1-deleted cells and reverts their hypersensitivity to DNA-damaging agents. We find reduced 53BP1 expression in subsets of sporadic triple-negative and BRCA-associated breast cancers, indicating the potential clinical implications of our findings.

Citace poskytuje Crossref.org

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