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Zoledronic Acid Inhibits Cancer Growth (Paperback)
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Zoledronic Acid Inhibits Cancer Growth (Paperback)
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PMThe aminobisphosphonate zoledronic acid(ZOL) has elicited
significant attention due to its remarkable anti-tumoral
activity,though its detailed mechanism of action remains unclear.
Here,we demonstrate the existence of a nuclear GSK3-NFATc2
stabilization pathway that promotes cancer growth in vitro and in
vivo and serves as a bonafide target of ZOL. Specifically, the
serine/threonine kinase GSK3 stabilizes nuclear NFATc2 through
phosphorylation of the serine-rich SP2 domain, thus protecting the
transcription factor from E3-ubiquitin ligase HDM2 mediated
proteolysis. ZOL disrupts this NFATc2 stabilization pathway through
two mechanisms, namely GSK3 inhibition and induction of HDM2
activity. Upon nuclear accumulation,HDM2 targets unphosphorylated
NFATc2 for ubiquitination at acceptor lysine residues K-684/K-897
and hence labels the factor for subsequent proteasomal degradation.
Conversely, mutagenesis induced constitutive serine phosphorylation
of the SP2 domain prevents NFATc2 from HDM2 mediated ubiquitination
and degradation by ZOL. In conclusion, this report demonstrates a
critical role of the GSK3-HDM2 signaling loop in the regulation of
NFATc2 protein stabilit
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