Transforming properties of YAP, a candidate oncogene on the chromosome 11q22 amplicon

By M. Overholtzer, Jianmin Zhang, G. Smolen, Beth Muir, Wenmei Li, D. Sgroi, C. Deng, J. Brugge, D. Haber. Proceedings of the National Academy of Sciences of the United States of America, 2006

969 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/e4b12c9b774877c65ac62d19e1177a5eaebb164c

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In Cell Biology

1. K. Guan
2. G. Halder
3. Bin Zhao
4. Duojia Pan
5. Fa-Xing Yu
6. S. Piccolo
7. Randy L. Johnson
8. M. Cordenonsi

In Molecular Biology

1. K. Guan
2. Duojia Pan
3. Bin Zhao
4. G. Halder
5. Fa-Xing Yu
6. Randy L. Johnson
7. S. Piccolo
8. M. Cordenonsi

In Oncology

1. Brent R. Stockwell
2. J. Massagué
3. K. Guan
4. Duojia Pan
5. S. Piccolo
6. Xuejun Jiang
7. Bin Zhao
8. J. Brugge

Citations in the corpus

• Hippo signaling: growth control and beyond (2011, background): “…et al., 2008; Harvey et al., 2003; Huang et al., 2005; Jia et al., 2003; Kango-Singh et al., 2002; Neto-Silva et al., 2010; Nolo et al., 2006; Pantalacci et al., 2003; Peng et al., 2009; Tapon et al., 2002; Thompson and Cohen, 2006; Udan et al., 2003; Wu et al., 2003; Wu et al., 2008; Zhang…”
• The TEAD/TEF family protein Scalloped mediates transcriptional output of the Hippo growth-regulatory pathway. (2008, background): “YAP, the mammalian homolog of yki, is amplified in certain tumors and can transform immortalized mammary epithelial cells in vitro (Overholtzer et al., 2006) and accelerate tumorigenesis in conjunction with p53 loss and c-myc overexpression (Zender et al.”
• Inactivation of YAP oncoprotein by the Hippo pathway is involved in cell contact inhibition and tissue growth control. (2007, background): “Interestingly, YAP has been shown recently to be a candidate oncogene in the human chromosome 11q22 amplicon (Overholtzer et al. 2006; Zender et al. 2006).”
• The Hippo Signaling Pathway in Development and Disease (2019, background): “First, amplification of the YAP gene locus occurs in various cancers including CSCC, hepatocellular carcinoma, medulloblastoma, and oral squamous cell carcinoma (Fernandez-L et al., 2009; Overholtzer et al., 2006; Wang et al., 2018b; Zender et al., 2006).”
• Elucidation of a universal size-control mechanism in Drosophila and mammals. (2007, background): “For example, YAP was recently shown to transform immortalized mammary epithelial cells in vitro (Overholtzer et al., 2006) and to accelerate tumorigenesis in conjunction with p53 loss and c-myc overexpression (Zender et al.”
• The Hippo pathway: regulators and regulations. (2013, background): “YAP and TAZ induced an epithelial–mesenchymal transition (EMT), a phenomenon crucial for the initiation of cancer metastasis (Overholtzer et al. 2006; Lei et al. 2008; Thiery et al. 2009).”
• The Hippo pathway in organ size control, tissue regeneration and stem cell self-renewal (2011, neutral): “Genomic amplification of YAP is also observed in human cancers and a mouse model of breast cance”
• The two faces of Hippo: targeting the Hippo pathway for regenerative medicine and cancer treatment (2013, positive): “Thus, YAP/TAZ activation by loss of cell polarity may engage a positive feed-forward loop in which YAP/TAZ promotes EMT and loss of cell polarity, which then further activates YAP and TAZ.”
• Cell detachment activates the Hippo pathway via cytoskeleton reorganization to induce anoikis. (2012, background): “Therefore, YAP-induced EMT and Erk activation may contribute to the function of YAP in inhibiting anoikis.”
• The Merlin/NF2 tumor suppressor functions through the YAP oncoprotein to regulate tissue homeostasis in mammals (2010, background): “Interestingly, the evidence so far implicating Hippo signaling in mammalian tissue homeostasis are largely based on YAP gain-of-function contexts, wherein gene amplification (Zender et al., 2006; Overholtzer et al., 2006), transgenic overexpression of YAP (Dong et al.”
• Mst1 and Mst2 maintain hepatocyte quiescence and suppress the development of hepatocellular carcinoma through inactivation of the Yap1 oncogene (2009, neutral): “Yap1 is amplified in a number of human tumor types and transgenic overexpression of Yap1 in mice leads to liver overgrowth and HCC as well as expansion of progenitor cells in multiple organs (Camargo et al., 2007; Dong et al., 2007; Overholtzer et al., 2006; Zender et al., 2006).”
• Regulation of the Hippo-YAP pathway by G-protein coupled receptor signaling (2012, background): “Moreover, abnormal activation of YAP and TAZ has been associated with human cancers (Overholtzer et al., 2006; Steinhardt et al., 2008; Zender et al., 2006; Zhao et al., 2007), suggesting an important role for the Hippo pathway in tumorigenesis.”
• The Hippo-YAP pathway in organ size control and tumorigenesis: an updated version. (2010, background): “More interestingly, two reports identified YAP as a driving oncogene in human HCC and breast cancer 11q22 amplicons (Overholtzer et al. 2006; Zender et al. 2006).”
• The biology of YAP/TAZ: hippo signaling and beyond. (2014, background): “This function is conserved in mammalian cells: overexpression of nonphosphorylatable forms of YAP or TAZ increases the proliferation of several human or mouse cell lines in vitro (114, 165, 167, 267).”
• The role of YAP transcription coactivator in regulating stem cell self-renewal and differentiation. (2010, background): “YAP is an oncogene located in the human amplicon 11q22 (Overholtzer et al. 2006; Zender et al. 2006).”
• TEAD mediates YAP-dependent gene induction and growth control. (2008, background): “YAP overexpression is reported to induce anchorage-independent growth of MCF10A cells (Overholtzer et al. 2006).”
• The Hippo signaling pathway in stem cell biology and cancer (2014, neutral): “In addition, YAP gene amplification (somatic mutation) has been reported in various human and murine tumor models [136,141].”
• TAZ Promotes Cell Proliferation and Epithelial-Mesenchymal Transition and Is Inhibited by the Hippo Pathway (2008, background): “The morphological alterations were also confirmed by phalloidin staining for F-actin, which is another hallmark of EMT, indicating disorganization of adherens junctions (22).”