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• W1844282257 startingPage "130" @default.
• W1844282257 abstract "The protein kinase Aurora-A is a major regulator of the cell cycle that orchestrates mitotic entry and is required for the assembly of a functional mitotic spindle. Overexpression of Aurora-A has been strongly linked with oncogenesis and this has led to considerable efforts at therapeutic targeting of the kinase activity of this protein. However, the exact mechanism by which Aurora-A promotes oncogenesis remains unclear. Here, we show that Aurora-A modulates the repair of DNA double-strand breaks (DSBs). Aurora-A expression inhibits RAD51 recruitment to DNA DSBs, decreases DSB repair by homologous recombination and sensitizes cancer cells to PARP inhibition. This impairment of RAD51 function requires inhibition of CHK1 by Polo-like kinase 1 (PLK1). These results identify a novel function of Aurora-A in modulating the response to DNA DSB that likely contributes to carcinogenesis and suggest a novel therapeutic approach to the treatment of cancers overexpressing this protein." @default.
• W1844282257 created "2016-06-24" @default.
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• W1844282257 date "2010-04-01" @default.
• W1844282257 modified "2023-10-13" @default.
• W1844282257 title "Aurora‐A expressing tumour cells are deficient for homology‐directed DNA double strand‐break repair and sensitive to PARP inhibition" @default.
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• W1844282257 doi "https://doi.org/10.1002/emmm.201000068" @default.
• W1844282257 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3377280" @default.
• W1844282257 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20373286" @default.
• W1844282257 hasPublicationYear "2010" @default.
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