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Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Biol+Chem 2017 ; 292 (13): 5253-61 Nephropedia Template TP
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Metformin Promotes AMP-activated Protein Kinase-independent Suppression of ?Np63? Protein Expression and Inhibits Cancer Cell Viability* #MMPMID28193839
Yi Y; Chen D; Ao J; Sun S; Wu M; Li X; Bergholz J; Zhang Y; Xiao ZX
J Biol Chem 2017[Mar]; 292 (13): 5253-61 PMID28193839show ga
The blood glucose modifier metformin is used to treat type II diabetes and has also been shown to possess anticancer activities. Recent studies indicate that glucose deprivation can greatly enhance metformin-mediated inhibition of cell viability, but the molecular mechanism involved in this inhibition is unclear. In this study, we report that, under glucose deprivation, metformin inhibited expression of ?Np63?, a p53 family member involved in cell adhesion pathways, resulting in disruption of cell matrix adhesion and subsequent apoptosis in human squamous carcinoma cells. We further show that metformin promoted ?Np63? protein instability independent of AMP-activated protein kinase and that WWP1, an E3 ligase of ?Np63?, was involved in metformin-mediated down-regulation of ?Np63? levels. In addition, we demonstrate that a combination of metformin and the glycolysis inhibitor 2-deoxy-d-glucose significantly inhibited ?Np63? expression and also suppressed xenographic tumor growth in vivo. In summary, this study reveals a new mechanism for metformin-mediated anticancer activity and suggests a new strategy for treating human squamous cell carcinoma.