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10.1038/ncomms15289 http://scihub22266oqcxt.onion/10.1038/ncomms15289 C5424153!5424153!28474672     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=28474672|t=2017. Stat3 regulates centrosome clustering in cancer cells via Stathmin/PLK1 |pdf=|usr=}}{{28474672}} gab.com Text Stat3 regulates centrosome clustering in cancer cells via Stathmin/PLK1 JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28474672 #FOAvip Cancer cells frequently have amplified centrosomes that must be clustered together to form a bipolar mitotic spindle, and targeting centrosome clustering is considered a promising therapeutic strategy. A high-content chemical screen for inhibitors of centrosome clustering identified Stattic, a Stat3 inhibitor. Stat3 depletion and inhibition in cancer cell lines and in tumours in vivo caused significant inhibition of centrosome clustering and viability. Here we describe a transcription-independent mechanism for Stat3-mediated centrosome clustering that involves Stathmin, a Stat3 interactor involved in microtubule depolymerization, and the mitotic kinase PLK1. Furthermore, PLK4-driven centrosome amplified breast tumour cells are highly sensitive to Stat3 inhibitors. We have identified an unexpected role of Stat3 in the regulation of centrosome clustering, and this role of Stat3 may be critical in identifying tumours that are sensitive to Stat3 inhibitors. Twit Text FOAVip Stat3 regulates centrosome clustering in cancer cells via Stathmin/PLK1 ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28474672 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28474672 #FOAvip English Wikipedia <ref>{{Cite pmid|28474672}}</ref> Stat3 regulates centrosome clustering in cancer cells via Stathmin/PLK1 #MMPMID28474672 Morris EJ; Kawamura E; Gillespie JA; Balgi A; Kannan N; Muller WJ; Roberge M; Dedhar S Nat Commun 2017[]; 8 (ä): ä PMID28474672show ga Cancer cells frequently have amplified centrosomes that must be clustered together to form a bipolar mitotic spindle, and targeting centrosome clustering is considered a promising therapeutic strategy. A high-content chemical screen for inhibitors of centrosome clustering identified Stattic, a Stat3 inhibitor. Stat3 depletion and inhibition in cancer cell lines and in tumours in vivo caused significant inhibition of centrosome clustering and viability. Here we describe a transcription-independent mechanism for Stat3-mediated centrosome clustering that involves Stathmin, a Stat3 interactor involved in microtubule depolymerization, and the mitotic kinase PLK1. Furthermore, PLK4-driven centrosome amplified breast tumour cells are highly sensitive to Stat3 inhibitors. We have identified an unexpected role of Stat3 in the regulation of centrosome clustering, and this role of Stat3 may be critical in identifying tumours that are sensitive to Stat3 inhibitors. äStat3 regulates centrosome clustering in cancer cells via Stathmin/PLK(epmc).pdf DeepDyve Pubget Overpricing