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10.18632/oncotarget.18488 http://scihub22266oqcxt.onion/10.18632/oncotarget.18488 C5601624!5601624!28938528     free     free     free       Oncotarget 2017 ; 8 (35): 57938-47 Nephropedia Template TP {{tp|p=28938528|t=2017. p53-independent p21 induction by MELK inhibition |pdf=|usr=}}{{28938528}} gab.com Text p53-independent p21 induction by MELK inhibition JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28938528 #FOAvip MELK play critical roles in human carcinogenesis through activation of cell proliferation, inhibition of apoptosis and maintenance of stemness. Therefore, MELK is a promising therapeutic target for a wide range of cancers. Although p21 is a well-known p53-downstream gene, we found that treatment with a potent MELK inhibitor, OTS167, could induce p21 protein expression in cancer cell lines harboring loss-of-function TP53 mutations. We also confirmed that MELK knockdown by siRNA induced the p21 expression in p53-deficient cancer cell lines and caused the cell cycle arrest at G1 phase. Further analysis indicated that FOXO1 and FOXO3, two known transcriptional regulators of p21, were phosphorylated by MELK and thus be involved in the induction of p21 after MELK inhibition. Collectively, our herein findings suggest that MELK inhibition may be effective for human cancers even if TP53 is mutated. Twit Text FOAVip p53-independent p21 induction by MELK inhibition ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28938528 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28938528 #FOAvip English Wikipedia <ref>{{Cite pmid|28938528}}</ref> p53-independent p21 induction by MELK inhibition #MMPMID28938528 Matsuda T; Kato T; Kiyotani K; Tarhan YE; Saloura V; Chung S; Ueda K; Nakamura Y; Park JH Oncotarget 2017[Aug]; 8 (35): 57938-47 PMID28938528show ga MELK play critical roles in human carcinogenesis through activation of cell proliferation, inhibition of apoptosis and maintenance of stemness. Therefore, MELK is a promising therapeutic target for a wide range of cancers. Although p21 is a well-known p53-downstream gene, we found that treatment with a potent MELK inhibitor, OTS167, could induce p21 protein expression in cancer cell lines harboring loss-of-function TP53 mutations. We also confirmed that MELK knockdown by siRNA induced the p21 expression in p53-deficient cancer cell lines and caused the cell cycle arrest at G1 phase. Further analysis indicated that FOXO1 and FOXO3, two known transcriptional regulators of p21, were phosphorylated by MELK and thus be involved in the induction of p21 after MELK inhibition. Collectively, our herein findings suggest that MELK inhibition may be effective for human cancers even if TP53 is mutated. äp53-independent p21 induction by MELK inhibition (epmc).pdf DeepDyve Pubget Overpricing