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• W2062593619 abstract "Summary SYK tyrosine kinase has emerged as a master regulator of cellular resistance to oxidative stress (OS) by mediating the activation of the anti‐apoptotic nuclear factor κB and phosphatidylinositol‐3 kinase/AKT pathways after OS exposure. Here, we present unprecedented experimental evidence that polo‐like kinase 1 (PLK1) is the upstream regulator of SYK in B‐lineage acute lymphoblastic leukaemia (ALL) cells. Selective inhibition of PLK‐1 with the leflunomide metabolite analogue α‐cyano‐β‐hydroxy‐β‐methyl‐ N ‐[4‐(trifluoromethoxy) phenyl]‐propenamide/LFM‐A12 abolished the resistance of B‐lineage ALL cells to OS by preventing the activation of the anti‐apoptotic SYK signal transduction pathway. Notably, LFM‐A12 treatments at non‐cytotoxic concentrations resulted in marked augmentation of clonogenic death in resistant human B‐lineage ALL cell lines challenged with OS. Further, LFM‐A12 augmented OS‐induced apoptosis of chemotherapy‐resistant primary leukaemic cells from relapsed B‐lineage ALL patients in vitro and markedly potentiated the in vivo anti‐leukaemic activity of total body irradiation (TBI) against leukaemia‐initiating cells in severe combined immunodeficient mouse xenograft models of B‐lineage ALL. This study is the first to identify PLK1 as a regulator of SYK tyrosine kinase and a molecular target to overcome SYK‐mediated resistance of B‐lineage ALL cells to OS." @default.
• W2062593619 created "2016-06-24" @default.
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• W2062593619 date "2010-02-09" @default.
• W2062593619 modified "2023-10-18" @default.
• W2062593619 title "Polo-like-kinase 1 (PLK1) as a molecular target to overcome SYK-mediated resistance of B-lineage acute lymphoblastic leukaemia cells to oxidative stress" @default.
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• W2062593619 doi "https://doi.org/10.1111/j.1365-2141.2009.07983.x" @default.
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