YAP1 mediates survival of ALK-rearranged lung cancer cells treated with alectinib via pro-apoptotic protein regulation

[1]  Jing Wang,et al.  WebGestalt 2019: gene set analysis toolkit with revamped UIs and APIs , 2019, Nucleic Acids Res..

[2]  S. Yano,et al.  AXL confers intrinsic resistance to osimertinib and advances the emergence of tolerant cells , 2019, Nature Communications.

[3]  Young Hak Kim,et al.  Alectinib Resistance in ALK-Rearranged Lung Cancer by Dual Salvage Signaling in a Clinically Paired Resistance Model , 2018, Molecular Cancer Research.

[4]  C. Alidousty.  Genetic instability and recurrent MYC amplification in ALK-translocated NSCLC; a central role of TP53 mutations , 2018 .

[5]  Jason V. Evans,et al.  Notch3-dependent β-catenin signaling mediates EGFR TKI drug persistence in EGFR mutant NSCLC , 2018, Nature Communications.

[6]  J. Wolf,et al.  Genetic instability and recurrent MYC amplification in ALK‐translocated NSCLC: a central role of TP53 mutations , 2018, The Journal of pathology.

[7]  A. Stemmer-Rachamimov,et al.  Programming of Schwann Cells by Lats1/2-TAZ/YAP Signaling Drives Malignant Peripheral Nerve Sheath Tumorigenesis. , 2018, Cancer cell.

[8]  J. Ajani,et al.  A Novel YAP1 Inhibitor Targets CSC-Enriched Radiation-Resistant Cells and Exerts Strong Antitumor Activity in Esophageal Adenocarcinoma , 2017, Molecular Cancer Therapeutics.

[9]  Young Hak Kim,et al.  Alectinib versus crizotinib in patients with ALK-positive non-small-cell lung cancer (J-ALEX): an open-label, randomised phase 3 trial , 2017, The Lancet.

[10]  Rafal Dziadziuszko,et al.  Alectinib versus Crizotinib in Untreated ALK‐Positive Non–Small‐Cell Lung Cancer , 2017, The New England journal of medicine.

[11]  S. Giulitti,et al.  YAP/TAZ link cell mechanics to Notch signalling to control epidermal stem cell fate , 2017, Nature Communications.

[12]  A. Cuadrado,et al.  Mutant p53 oncogenic functions in cancer stem cells are regulated by WIP through YAP/TAZ , 2017, Oncogene.

[13]  Lauren L. Ritterhouse,et al.  Molecular Mechanisms of Resistance to First- and Second-Generation ALK Inhibitors in ALK-Rearranged Lung Cancer. , 2016, Cancer discovery.

[14]  Masaki Matsumoto,et al.  jPOSTrepo: an international standard data repository for proteomes , 2016, Nucleic Acids Res..

[15]  Lauren L. Ritterhouse,et al.  Molecular Mechanisms of Resistance to First- and Second-Generation ALK Inhibitors in ALK-Rearranged Lung Cancer , 2016 .

[16]  John D. Minna,et al.  XPO1-dependent nuclear export is a druggable vulnerability in KRAS-mutant lung cancer , 2016, Nature.

[17]  G. Longmore,et al.  AJUBA LIM Proteins Limit Hippo Activity in Proliferating Cells by Sequestering the Hippo Core Kinase Complex in the Cytosol , 2016, Molecular and Cellular Biology.

[18]  S. Uccini,et al.  High prevalence of ALK+/ROS1+ cases in pulmonary adenocarcinoma of adoloscents and young adults. , 2016, Lung cancer.

[19]  K. Kiura,et al.  Non-Small Cell Lung Cancer Cells Acquire Resistance to the ALK Inhibitor Alectinib by Activating Alternative Receptor Tyrosine Kinases. , 2016, Cancer research.

[20]  S. Bicciato,et al.  YAP enhances the pro‐proliferative transcriptional activity of mutant p53 proteins , 2016, EMBO reports.

[21]  G. Getz,et al.  Resensitization to Crizotinib by the Lorlatinib ALK Resistance Mutation L1198F. , 2016, The New England journal of medicine.

[22]  Xiao Han,et al.  Targeting the Central Pocket in Human Transcription Factor TEAD as a Potential Cancer Therapeutic Strategy. , 2015, Structure.

[23]  B. Taylor,et al.  NF2 Loss Promotes Oncogenic RAS-Induced Thyroid Cancers via YAP-Dependent Transactivation of RAS Proteins and Sensitizes Them to MEK Inhibition. , 2015, Cancer discovery.

[24]  Junjie Chen,et al.  Tankyrase Inhibitors Target YAP by Stabilizing Angiomotin Family Proteins. , 2015, Cell reports.

[25]  I. Garraway,et al.  YAP1 and AR interactions contribute to the switch from androgen-dependent to castration-resistant growth in prostate cancer , 2015, Nature Communications.

[26]  I. Clay,et al.  YAP1 Exerts Its Transcriptional Control via TEAD-Mediated Activation of Enhancers , 2015, PLoS genetics.

[27]  D. Coppola,et al.  YAP1 Regulates OCT4 Activity and SOX2 Expression to Facilitate Self‐Renewal and Vascular Mimicry of Stem‐Like Cells , 2015, Stem cells.

[28]  K. Kuroda,et al.  Elucidation of the recognition mechanisms for hemicellulose and pectin in Clostridium cellulovorans using intracellular quantitative proteome analysis , 2015, AMB Express.

[29]  K. Okuno,et al.  Activated MET acts as a salvage signal after treatment with alectinib, a selective ALK inhibitor, in ALK-positive non-small cell lung cancer. , 2015, International journal of oncology.

[30]  H. Sasaki,et al.  Cell competition in mouse NIH3T3 embryonic fibroblasts is controlled by the activity of Tead family proteins and Myc , 2015, Journal of Cell Science.

[31]  Kun-Liang Guan,et al.  The emerging roles of YAP and TAZ in cancer , 2015, Nature Reviews Cancer.

[32]  Sridhar Ramaswamy,et al.  Patient-derived models of acquired resistance can identify effective drug combinations for cancer , 2014, Science.

[33]  D. Carbone,et al.  EGFR blockade enriches for lung cancer stem-like cells through Notch3-dependent signaling. , 2014, Cancer research.

[34]  A. Iafrate,et al.  Two Novel ALK Mutations Mediate Acquired Resistance to the Next-Generation ALK Inhibitor Alectinib , 2014, Clinical Cancer Research.

[35]  K. Guan,et al.  The Hippo signaling pathway in stem cell biology and cancer , 2014, EMBO reports.

[36]  A. Rosato,et al.  Metabolic control of YAP and TAZ by the mevalonate pathway , 2014, Nature Cell Biology.

[37]  Toyokawa Gouji,et al.  Crizotinib can overcome acquired resistance to CH5424802: is amplification of the MET gene a key factor? , 2014, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[38]  Jae Ho Lee,et al.  Comparison of clinical characteristics between patients with ALK-positive and EGFR-positive lung adenocarcinoma. , 2014, Respiratory medicine.

[39]  Lin Mei,et al.  Interplay of mevalonate and Hippo pathways regulates RHAMM transcription via YAP to modulate breast cancer cell motility , 2013, Proceedings of the National Academy of Sciences.

[40]  Y. Morimoto,et al.  Hippo signaling disruption and Akt stimulation of ovarian follicles for infertility treatment , 2013, Proceedings of the National Academy of Sciences.

[41]  S. Krauss,et al.  Tankyrases as drug targets , 2013, The FEBS journal.

[42]  Y. Ohe,et al.  CH5424802 (RO5424802) for patients with ALK-rearranged advanced non-small-cell lung cancer (AF-001JP study): a single-arm, open-label, phase 1-2 study. , 2013, The Lancet. Oncology.

[43]  S. Krauss,et al.  A novel tankyrase small-molecule inhibitor suppresses APC mutation-driven colorectal tumor growth. , 2013, Cancer research.

[44]  J. Mesirov,et al.  β-Catenin-Driven Cancers Require a YAP1 Transcriptional Complex for Survival and Tumorigenesis , 2013, Cell.

[45]  David M. Thomas,et al.  The Hippo pathway and human cancer , 2013, Nature Reviews Cancer.

[46]  Jill P. Mesirov,et al.  β-Catenin-Driven Cancers Require a YAP1 Transcriptional Complex for Survival and Tumorigenesis , 2012, Cell.

[47]  Stefano Piccolo,et al.  Transduction of mechanical and cytoskeletal cues by YAP and TAZ , 2012, Nature Reviews Molecular Cell Biology.

[48]  F. Camargo,et al.  The Hippo signaling pathway and stem cell biology. , 2012, Trends in cell biology.

[49]  Jun O. Liu,et al.  Genetic and pharmacological disruption of the TEAD-YAP complex suppresses the oncogenic activity of YAP. , 2012, Genes & development.

[50]  Carol Prives,et al.  Mutant p53: one name, many proteins. , 2012, Genes & development.

[51]  J. Moult,et al.  Structural and functional impact of cancer-related missense somatic mutations. , 2011, Journal of molecular biology.

[52]  T. Okano,et al.  Hippo pathway regulation by cell morphology and stress fibers , 2011, Development.

[53]  Nicola Elvassore,et al.  Role of YAP/TAZ in mechanotransduction , 2011, Nature.

[54]  Hiroshi Sakamoto,et al.  CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. , 2011, Cancer cell.

[55]  Ryohei Katayama,et al.  Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK , 2011, Proceedings of the National Academy of Sciences.

[56]  J. McDonald,et al.  A practical guide to evaluating colocalization in biological microscopy. , 2011, American journal of physiology. Cell physiology.

[57]  O. Kirak,et al.  Yap1 Acts Downstream of α-Catenin to Control Epidermal Proliferation , 2011, Cell.

[58]  Jun Yu,et al.  Yes-Associated Protein 1 Exhibits Oncogenic Property in Gastric Cancer and Its Nuclear Accumulation Associates with Poor Prognosis , 2011, Clinical Cancer Research.

[59]  H. Pasolli,et al.  Yes-associated protein (YAP) transcriptional coactivator functions in balancing growth and differentiation in skin , 2011, Proceedings of the National Academy of Sciences.

[60]  D. Pan.  The hippo signaling pathway in development and cancer. , 2010, Developmental cell.

[61]  A. Gemma,et al.  F1000 highlights , 2010 .

[62]  H. Aburatani,et al.  Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer , 2007, Nature.

[63]  David H. Johnson,et al.  Randomized phase II trial of paclitaxel plus carboplatin or gemcitabine plus cisplatin in Eastern Cooperative Oncology Group performance status 2 non-small-cell lung cancer patients: ECOG 1599. , 2007, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[64]  N. Saijo,et al.  Randomized phase III study of cisplatin plus irinotecan versus carboplatin plus paclitaxel, cisplatin plus gemcitabine, and cisplatin plus vinorelbine for advanced non-small-cell lung cancer: Four-Arm Cooperative Study in Japan. , 2006, Annals of oncology : official journal of the European Society for Medical Oncology.

[65]  G. Blandino,et al.  The transcriptional coactivator Yes-associated protein drives p73 gene-target specificity in response to DNA Damage. , 2005, Molecular cell.

[66]  S. Gabriel,et al.  EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy , 2004, Science.

[67]  J. Herz.  Faculty Opinions recommendation of EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. , 2004 .

[68]  D. Wessel,et al.  A method for the quantitative recovery of protein in dilute solution in the presence of detergents and lipids. , 1984, Analytical biochemistry.

[69]  Jindan Yu,et al.  Cell detachment activates the Hippo pathway via cytoskeleton reorganization to induce anoikis. , 2012, Genes & development.

[70]  J. Downward,et al.  Akt phosphorylates the Yes-associated protein, YAP, to induce interaction with 14-3-3 and attenuation of p73-mediated apoptosis. , 2003, Molecular cell.

[71]  Susumu Goto,et al.  KEGG: Kyoto Encyclopedia of Genes and Genomes , 2000, Nucleic Acids Res..

[72]  Supplemental Information 2: Kyoto Encyclopedia of genes and genomes. , 2022 .