S100A7 induction is repressed by YAP via the Hippo pathway in A431 cells
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Yunguang Li1,*, Fei Kong1,*, Junhao Wang,1 Enze Hu,1 Rui Wang,1 Jin Liu,1 Qianqian Xiao,1 Weiqing Zhang,1 Dacheng He,1 Xueyuan Xiao1
1Key Laboratory of Cell Proliferation and Regulation Biology, Ministry of Education, Beijing Normal University, Beijing, China
*These authors contributed equally to this work
Xueyuan Xiao, email: [email protected]
Keywords: S100A7, YAP, Hippo pathway, F-actin, A431
Received: March 10, 2016 Accepted: April 27, 2016 Published: May 19, 2016
YAP is an oncogenic transcriptional co-activator and is inhibited by the Hippo pathway. Recent studies have revealed that YAP is also a sensor of cell morphology and cell density and can be phosphorylated by cytoskeleton reorganization. Our previous study demonstrated that S100A7 was upregulated in several squamous cell carcinoma (SCC) specimens and was dramatically induced in SCC cells by suspension and dense culture as well as in xenografts. However, little is known about how S100A7 induction occurs in cancer cells. Here, we identify that S100A7 induction is accompanied by YAP phosphorylation in both suspended and dense A431 cells. This correlation reverses after recovery of cell attachment or relief from dense culture. Further examination finds that S100A7 induction is repressed by nuclear YAP, which is further validated by activation or inhibition of the Hippo pathway via loss- and/or gain-of- LATS1 and MST1 function. Strikingly, disruption of the F-actin promotes S100A7 expression via YAP by activation of the Hippo pathway. Furthermore, we demonstrate that repression of S100A7 by YAP required TEAD1 transcriptional factor. Taken together, our findings demonstrate for the first time that S100A7 is repressed by YAP via the Hippo pathway.
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