Silencing Notch4 promotes tumorigenesis and inhibits metastasis of triple-negative breast cancer via Nanog and Cdc42

[1]  Xiaolong Wei,et al.  Notch3 Transactivates Glycogen Synthase Kinase-3-Beta and Inhibits Epithelial-to-Mesenchymal Transition in Breast Cancer Cells , 2022, Cells.

[2]  Kongming Wu,et al.  Notch signaling pathway: architecture, disease, and therapeutics , 2022, Signal Transduction and Targeted Therapy.

[3]  G. Christofori,et al.  Distinct contributions of partial and full EMT to breast cancer malignancy. , 2021, Developmental cell.

[4]  M. Teh,et al.  Vimentin Is at the Heart of Epithelial Mesenchymal Transition (EMT) Mediated Metastasis , 2021, Cancers.

[5]  I. Mayer,et al.  A Phase Ib Dose Escalation Trial of RO4929097 (a γ-secretase inhibitor) in Combination with Exemestane in Patients with ER + Metastatic Breast Cancer (MBC) , 2021, Clinical Breast Cancer.

[6]  T. Brabletz,et al.  Dynamic EMT: a multi‐tool for tumor progression , 2021, The EMBO journal.

[7]  Antony K. Chen,et al.  A Background Assessable and Correctable Bimolecular Fluorescence Complementation System for Nanoscopic Single-Molecule Imaging of Intracellular Protein-Protein Interactions. , 2021, ACS nano.

[8]  S. Puram,et al.  Partial EMT in head and neck cancer biology: a spectrum instead of a switch , 2021, Oncogene.

[9]  Wen-He Huang,et al.  Notch3 inhibits cell proliferation and tumorigenesis and predicts better prognosis in breast cancer through transactivating PTEN , 2021, Cell Death & Disease.

[10]  R. Weinberg,et al.  Linking EMT programmes to normal and neoplastic epithelial stem cells , 2021, Nature Reviews Cancer.

[11]  Zhengxu Fang,et al.  Regulatory mechanisms and clinical significance of vimentin in breast cancer. , 2021, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.

[12]  Käthe M. Dahlström,et al.  PIM-induced phosphorylation of Notch3 promotes breast cancer tumorigenicity in a CSL-independent fashion , 2021, The Journal of biological chemistry.

[13]  J. Crabtree,et al.  Targeting Notch in oncology: the path forward , 2020, Nature Reviews Drug Discovery.

[14]  S. Köster,et al.  Vimentin intermediate filaments stabilize dynamic microtubules by direct interactions , 2020, Nature Communications.

[15]  Yuanyuan Qin,et al.  NOTCH4 maintains quiescent mesenchymal-like breast cancer stem cells via transcriptionally activating SLUG and GAS1 in triple-negative breast cancer , 2020, Theranostics.

[16]  M. Grever,et al.  A phase I study of an oral selective gamma secretase (GS) inhibitor RO4929097 in combination with neoadjuvant paclitaxel and carboplatin in triple negative breast cancer , 2020, Investigational New Drugs.

[17]  R. Baffa,et al.  A phase I, dose-escalation study of PF-06650808, an anti-Notch3 antibody–drug conjugate, in patients with breast cancer and other advanced solid tumors , 2019, Investigational New Drugs.

[18]  L. Espinosa,et al.  The multiple usages of Notch signaling in development, cell differentiation and cancer. , 2018, Current opinion in cell biology.

[19]  J. Sarkaria,et al.  NOTCH3 expression is linked to breast cancer seeding and distant metastasis , 2018, Breast cancer research : BCR.

[20]  F. Kruyt,et al.  MiR-221/222 promote epithelial-mesenchymal transition by targeting Notch3 in breast cancer cell lines , 2018, npj Breast Cancer.

[21]  Wen-He Huang,et al.  Notch3 inhibits epithelial–mesenchymal transition in breast cancer via a novel mechanism, upregulation of GATA-3 expression , 2018, Oncogenesis.

[22]  Luke A. Torre-Healy,et al.  Cx26 drives self-renewal in triple-negative breast cancer via interaction with NANOG and focal adhesion kinase , 2018, Nature Communications.

[23]  M. Balasubramanian,et al.  Cell Polarity in Yeast. , 2017, Annual review of cell and developmental biology.

[24]  K. Man,et al.  Notch3 Maintains Luminal Phenotype and Suppresses Tumorigenesis and Metastasis of Breast Cancer via Trans-Activating Estrogen Receptor-α , 2017, Theranostics.

[25]  Sangyoon J. Han,et al.  Vimentin fibers orient traction stress , 2017, Proceedings of the National Academy of Sciences.

[26]  Matthew J. Brauer,et al.  Constitutive NOTCH3 Signaling Promotes the Growth of Basal Breast Cancers. , 2017, Cancer research.

[27]  J. Imura,et al.  KLF4 and NANOG are prognostic biomarkers for triple-negative breast cancer , 2017, Breast Cancer.

[28]  F. Radtke,et al.  Notch as a tumour suppressor , 2017, Nature Reviews Cancer.

[29]  G. Curigliano,et al.  Phase I study of the gamma secretase inhibitor PF-03084014 in combination with docetaxel in patients with advanced triple-negative breast cancer , 2016, Oncotarget.

[30]  X. Liu,et al.  Notch3 inhibits epithelial–mesenchymal transition by activating Kibra-mediated Hippo/YAP signaling in breast cancer epithelial cells , 2016, Oncogenesis.

[31]  Zhuo Gan,et al.  Vimentin Intermediate Filaments Template Microtubule Networks to Enhance Persistence in Cell Polarity and Directed Migration. , 2016, Cell systems.

[32]  R. Yelensky,et al.  Triple-negative breast cancers with amplification of JAK2 at the 9p24 locus demonstrate JAK2-specific dependence , 2016, Science Translational Medicine.

[33]  Chuanzhao Zhang,et al.  Hypoxia induces the breast cancer stem cell phenotype by HIF-dependent and ALKBH5-mediated m6A-demethylation of NANOG mRNA , 2016, Proceedings of the National Academy of Sciences.

[34]  Jinbo Chen,et al.  Self-renewal of CD133hi cells by IL6/Notch3 signalling regulates endocrine resistance in metastatic breast cancer , 2016, Nature Communications.

[35]  E. Loftus,et al.  Sleep deprivation and false confessions , 2016 .

[36]  Guo‐Jun Zhang,et al.  Notch3 overexpression causes arrest of cell cycle progression by inducing Cdh1 expression in human breast cancer cells , 2016, Cell cycle.

[37]  Daniel J. Lew,et al.  Polarity establishment requires localized activation of Cdc42 , 2015, The Journal of cell biology.

[38]  A. Howell,et al.  Anti-estrogen Resistance in Human Breast Tumors Is Driven by JAG1-NOTCH4-Dependent Cancer Stem Cell Activity , 2015, Cell reports.

[39]  M. Hitomi,et al.  Development of a Fluorescent Reporter System to Delineate Cancer Stem Cells in Triple‐Negative Breast Cancer , 2015, Stem cells.

[40]  G. Curigliano,et al.  Phase I dose-finding study of the gamma secretase inhibitor PF-03084014 (PF-4014) in combination with docetaxel in patients (pts) with advanced triple-negative breast cancer (TNBC). , 2015 .

[41]  S. Chin,et al.  BCL11A is a triple-negative breast cancer gene with critical functions in stem and progenitor cells , 2015, Nature Communications.

[42]  A. Jimeno,et al.  A Phase I, Dose-Finding Study in Patients with Advanced Solid Malignancies of the Oral γ-Secretase Inhibitor PF-03084014 , 2014, Clinical Cancer Research.

[43]  E. Appella,et al.  The pluripotency factor nanog promotes breast cancer tumorigenesis and metastasis , 2014, Oncogene.

[44]  J. Christensen,et al.  Synergistic Effect of the γ‐Secretase Inhibitor PF‐03084014 and Docetaxel in Breast Cancer Models , 2013, Stem cells translational medicine.

[45]  James X. Song,et al.  Phase I study of RO4929097, a gamma secretase inhibitor of Notch signaling, in patients with refractory metastatic or locally advanced solid tumors. , 2012, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[46]  A. Mogilner,et al.  Cell Polarity: Quantitative Modeling as a Tool in Cell Biology , 2012, Science.

[47]  S. Grinstein,et al.  Phosphatidylserine is polarized and required for proper Cdc42 localization and for development of cell polarity , 2011, Nature Cell Biology.

[48]  A. Capobianco,et al.  Notch signalling in solid tumours: a little bit of everything but not all the time , 2011, Nature Reviews Cancer.

[49]  R. Clarke,et al.  Regulation of breast cancer stem cell activity by signaling through the Notch4 receptor. , 2010, Cancer research.

[50]  Prashant Mali,et al.  Notch signaling activation in human embryonic stem cells is required for embryonic, but not trophoblastic, lineage commitment. , 2008, Cell stem cell.

[51]  Yujing Wang,et al.  Firefly Luciferase Complementation Imaging Assay for Protein-Protein Interactions in Plants1[C][W][OA] , 2007, Plant Physiology.

[52]  A. Fischer,et al.  Delta–Notch—and then? Protein interactions and proposed modes of repression by Hes and Hey bHLH factors , 2007, Nucleic acids research.

[53]  Ryoichiro Kageyama,et al.  The Hes gene family: repressors and oscillators that orchestrate embryogenesis , 2007, Development.

[54]  M. Lupien,et al.  Tumorigenesis and Neoplastic Progression Overexpression of Activated Murine Notch 1 and Notch 3 in Transgenic Mice Blocks Mammary Gland Development and Induces Mammary Tumors , 2022 .

[55]  Alexander van Oudenaarden,et al.  A system of counteracting feedback loops regulates Cdc42p activity during spontaneous cell polarization. , 2005, Developmental cell.

[56]  S. Etienne-Manneville,et al.  Cdc42 - the centre of polarity , 2004, Journal of Cell Science.

[57]  D. Nelson,et al.  Cdc42-interacting Protein 4 Mediates Binding of the Wiskott-Aldrich Syndrome Protein to Microtubules* , 2000, The Journal of Biological Chemistry.

[58]  M. Satoh,et al.  Cellular polarity correlates with vimentin distribution, but not to keratin, in human renal cell carcinoma cells in vitro. , 1994, Cell structure and function.

[59]  Y. Oda,et al.  NOTCH4 is a potential therapeutic target for triple-negative breast cancer. , 2014, Anticancer research.

[60]  Guangjin Pan,et al.  Nanog and transcriptional networks in embryonic stem cell pluripotency , 2007, Cell Research.