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10.18632/oncotarget.14564 http://scihub22266oqcxt.onion/10.18632/oncotarget.14564 C5355113!5355113!28086236     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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2017 ; 8 (8): 13476-87 Nephropedia Template TP {{tp|p=28086236|t=2017. RYK promotes the stemness of glioblastoma cells via the WNT/?-catenin pathway |pdf=|usr=}}{{28086236}} gab.com Text RYK promotes the stemness of glioblastoma cells via the WNT/ -catenin pathway JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28086236 #FOAvip Glioblastoma multiforme (GBM) is characterized by a strong self-renewal potential and a poor differentiation state. Since receptor-like tyrosine kinase (RYK) activates the WNT/?-catenin pathway essential for cancer stem cell maintenance, we evaluated its contribution in conferring stemness to GBM cells. Here, we report that Ryk (related-to-receptor tyrosine kinase), an atypical tyrosine kinase receptor, is upregulated in samples from GBM patients as well as in GSCs. Ryk overexpression confers stemness properties to GBM cells through the modulation of the canonical Wnt signaling and by promoting the activation of pluripotency-related transcription factor circuitry and neurosphere formation ability. In contrast, siRNA-mediated knockdown of Ryk expression suppresses this stem-like phenotype. Rescue experiments reveal that stemness-promoting activity of Ryk is attributable, at least in part, to ?-catenin stabilization. Furthermore, Ryk overexpression improves cell motility and anchorage independent cell growth. Taken together, our findings demonstrate that Ryk promotes stem cell-like and tumorigenic features to glioma cells its essential for the maintenance of GSCs and could be a target of novel therapies. Twit Text FOAVip RYK promotes the stemness of glioblastoma cells via the WNT/ -catenin pathway ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28086236 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28086236 #FOAvip English Wikipedia <ref>{{Cite pmid|28086236}}</ref> RYK promotes the stemness of glioblastoma cells via the WNT/?-catenin pathway #MMPMID28086236 Adamo A; Fiore D; De Martino F; Roscigno G; Affinito A; Donnarumma E; Puoti I; Vitiani LR; Pallini R; Quintavalle C; Condorelli G Oncotarget 2017[Feb]; 8 (8): 13476-87 PMID28086236show ga Glioblastoma multiforme (GBM) is characterized by a strong self-renewal potential and a poor differentiation state. Since receptor-like tyrosine kinase (RYK) activates the WNT/?-catenin pathway essential for cancer stem cell maintenance, we evaluated its contribution in conferring stemness to GBM cells. Here, we report that Ryk (related-to-receptor tyrosine kinase), an atypical tyrosine kinase receptor, is upregulated in samples from GBM patients as well as in GSCs. Ryk overexpression confers stemness properties to GBM cells through the modulation of the canonical Wnt signaling and by promoting the activation of pluripotency-related transcription factor circuitry and neurosphere formation ability. In contrast, siRNA-mediated knockdown of Ryk expression suppresses this stem-like phenotype. Rescue experiments reveal that stemness-promoting activity of Ryk is attributable, at least in part, to ?-catenin stabilization. Furthermore, Ryk overexpression improves cell motility and anchorage independent cell growth. Taken together, our findings demonstrate that Ryk promotes stem cell-like and tumorigenic features to glioma cells its essential for the maintenance of GSCs and could be a target of novel therapies. äRYK promotes the stemness of glioblastoma cells via the WNT/?-catenin (epmc).pdf DeepDyve Pubget Overpricing