![]() These findings identify a previously unknown oncogenic property of the spatially deregulated AURKA in tumorigenesis and provide a potential therapeutic opportunity to overcome kinase inhibitor resistance. RNP K) in the nucleus and acts as a transcription factor in a complex that induces a shift in MYC promoter usage and activates the MYC promoter.īlocking AURKA nuclear localization inhibits this newly discovered transactivating function of AURKA, sensitizing resistant BCSC to kinase inhibition. Instead, AURKA preferentially interacts with heterogeneous nuclear ribonucleoprotein K (hn. Unexpectedly, this function is independent of its kinase activity. Here we show that AURKA translocates to the nucleus and causes distinct oncogenic properties in malignant cells by enhancing breast cancer stem cell (BCSC) phenotype. Centrosome- localized mitotic Aurora kinase A (AURKA) facilitates G2/M events. Nuclear AURKA acquires kinase- independent transactivating function to enhance breast cancer stem cell phenotype.
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