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• W3124917967 startingPage "1677" @default.
• W3124917967 abstract "ABSTRACT v‐Src oncogene causes cell transformation through its strong tyrosine kinase activity. We have revealed that v‐Src‐mediated cell transformation occurs at a low frequency and it is attributed to mitotic abnormalities‐mediated chromosome instability. v‐Src directly phosphorylates Tyr‐15 of cyclin‐dependent kinase 1 (CDK1), thereby causing mitotic slippage and reduction in Eg5 inhibitor cytotoxicity. However, it is not clear whether v‐Src modifies cytotoxicities of the other anticancer drugs targeting cell division. In this study, we found that v‐Src restores cancer cell viability reduced by various microtubule‐targeting agents (MTAs), although v‐Src does not alter cytotoxicity of DNA‐damaging anticancer drugs. v‐Src causes mitotic slippage of MTAs‐treated cells, consequently generating proliferating tetraploid cells. We further demonstrate that v‐Src also restores cell viability reduced by a polo‐like kinase 1 (PLK1) inhibitor. Interestingly, treatment with Aurora kinase inhibitor strongly induces cell death when cells express v‐Src. These results suggest that the v‐Src modifies cytotoxicities of anticancer drugs targeting cell division. Highly activated Src‐induced resistance to MTAs through mitotic slippage might have a risk to enhance the malignancy of cancer cells through the increase in chromosome instability upon chemotherapy using MTAs." @default.
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• W3124917967 date "2021-01-19" @default.
• W3124917967 modified "2023-10-15" @default.
• W3124917967 title "The tyrosine kinase v‐Src modifies cytotoxicities of anticancer drugs targeting cell division" @default.
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• W3124917967 doi "https://doi.org/10.1111/jcmm.16270" @default.
• W3124917967 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7875926" @default.
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