Abstract：
:SnoN regulates multiple signaling pathways, including TGF-β/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 with 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.
journal_name
Dev Celljournal_title
Developmental cellauthors
Zhu Q,Le Scolan E,Jahchan N,Ji X,Xu A,Luo Kdoi
10.1016/j.devcel.2016.05.002subject
Has Abstractpub_date
2016-06-06 00:00:00pages
399-412issue
5eissn
1534-5807issn
1878-1551pii
S1534-5807(16)30246-5journal_volume
37pub_type
杂志文章abstract：:The adult, virgin mammary gland is a highly organized tree-like structure formed by ducts with hollowed lumen. Although lumen formation during pubertal development appears to involve apoptosis, the molecular mechanisms that regulate this process are not known. Here, we demonstrate that disruption of the BH3-only proap...
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