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10.1016/j.devcel.2016.05.002

http://scihub22266oqcxt.onion/10.1016/j.devcel.2016.05.002
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C4902294!4902294!27237790
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suck abstract from ncbi


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pmid27237790      Dev+Cell 2016 ; 37 (5): 399-412
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  • SnoN antagonizes the Hippo kinase complex to promote TAZ signaling during breast carcinogenesis #MMPMID27237790
  • Zhu Q; Le Scolan E; Jahchan N; Ji X; Xu A; Luo K
  • Dev Cell 2016[Jun]; 37 (5): 399-412 PMID27237790show ga
  • SnoN regulates multiple signaling pathways including TGF?/Smad and p53 and displays both pro-oncogenic and anti-oncogenic activities in human cancer. We have observed previously that both its intracellular localization and expression levels are sensitive to cell density, suggesting that it may crosstalk to Hippo signaling. Here we report that indeed SnoN interacts with multiple components of the Hippo pathway to inhibit the binding of Lats2 to TAZ and the subsequent phosphorylation of TAZ, leading to TAZ stabilization. Consistently, SnoN enhances the transcriptional and oncogenic activities of TAZ, and reducing SnoN decreases TAZ expression as well as malignant progression of breast cancer cells. Interestingly, SnoN itself is downregulated by Lats2 that is activated by the Scribble basolateral polarity protein. Thus, SnoN is a critical component of the Hippo regulatory network that receives signals from the tissue architecture and polarity to coordinate the activity of intracellular signaling pathways.
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