| Literature DB >> 31754005 |
Iván M Moya1,2, Stéphanie A Castaldo1, Laura Van den Mooter1, Soheil Soheily1, Leticia Sansores-Garcia1, Jelle Jacobs3, Inge Mannaerts4, Jun Xie1, Elisabeth Verboven1, Hanne Hillen1, Ana Algueró-Nadal1, Ruchan Karaman1, Matthias Van Haele5, Weronika Kowalczyk1, Maxime De Waegeneer3, Stefaan Verhulst4, Panagiotis Karras6, Leen van Huffel1, Lars Zender7,8,9, Jean-Christophe Marine6, Tania Roskams5, Randy Johnson10, Stein Aerts3, Leo A van Grunsven4, Georg Halder11.
Abstract
The Hippo signaling pathway and its two downstream effectors, the YAP and TAZ transcriptional coactivators, are drivers of tumor growth in experimental models. Studying mouse models, we show that YAP and TAZ can also exert a tumor-suppressive function. We found that normal hepatocytes surrounding liver tumors displayed activation of YAP and TAZ and that deletion of Yap and Taz in these peritumoral hepatocytes accelerated tumor growth. Conversely, experimental hyperactivation of YAP in peritumoral hepatocytes triggered regression of primary liver tumors and melanoma-derived liver metastases. Furthermore, whereas tumor cells growing in wild-type livers required YAP and TAZ for their survival, those surrounded by Yap- and Taz-deficient hepatocytes were not dependent on YAP and TAZ. Tumor cell survival thus depends on the relative activity of YAP and TAZ in tumor cells and their surrounding tissue, suggesting that YAP and TAZ act through a mechanism of cell competition to eliminate tumor cells.Entities:
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Year: 2019 PMID: 31754005 DOI: 10.1126/science.aaw9886
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728