Snail determines the therapeutic response to mTOR kinase inhibitors by transcriptional repression of 4E-BP1

[1]  N. Sonenberg,et al.  Translational Control in Cancer. , 2018, Cold Spring Harbor perspectives in biology.

[2]  N. Nikitakis Glimpses of the near future: a new generation of mTOR inhibitors. , 2017, Oral diseases.

[3]  Kecheng Zhang,et al.  Cooperative Targets of Combined mTOR/HDAC Inhibition Promote MYC Degradation , 2017, Molecular Cancer Therapeutics.

[4]  Shih-Han Kao,et al.  Snail controls proliferation of Drosophila ovarian epithelial follicle stem cells, independently of E-cadherin. , 2016, Developmental biology.

[5]  V. LeBleu,et al.  EMT Program is Dispensable for Metastasis but Induces Chemoresistance in Pancreatic Cancer , 2015, Nature.

[6]  A. Piecuch,et al.  The role of Snail1 transcription factor in colorectal cancer progression and metastasis , 2015, Contemporary oncology.

[7]  Q. She,et al.  AKT inhibition overcomes rapamycin resistance by enhancing the repressive function of PRAS40 on mTORC1/4E-BP1 axis , 2015, Oncotarget.

[8]  Dong Wang,et al.  An evolutionarily conserved DNA architecture determines target specificity of the TWIST family bHLH transcription factors , 2015, Genes & development.

[9]  N. Sonenberg,et al.  Targeting the eIF4F translation initiation complex: a critical nexus for cancer development. , 2015, Cancer research.

[10]  M. Konopleva,et al.  mTOR kinase inhibitors synergize with histone deacetylase inhibitors to kill B-cell acute lymphoblastic leukemia cells , 2014, Oncotarget.

[11]  R. Johnstone,et al.  Histone deacetylases and their inhibitors in cancer, neurological diseases and immune disorders , 2015, Nature Reviews Drug Discovery.

[12]  Q. She,et al.  Loss of 4E-BP1 function induces EMT and promotes cancer cell migration and invasion via cap-dependent translational activation of snail , 2014, Oncotarget.

[13]  N. Sonenberg,et al.  Phosphorylation of eIF4E promotes EMT and metastasis via translational control of SNAIL and MMP-3 , 2014, Oncogene.

[14]  A. Puisieux,et al.  Oncogenic roles of EMT-inducing transcription factors , 2014, Nature Cell Biology.

[15]  B. Zhou,et al.  Epigenetic regulation of EMT: the Snail story. , 2014, Current pharmaceutical design.

[16]  J. Pelletier,et al.  Pancreatic tumours escape from translational control through 4E-BP1 loss , 2014, Oncogene.

[17]  C. Benz,et al.  mTORC1/C2 and pan-HDAC inhibitors synergistically impair breast cancer growth by convergent AKT and polysome inhibiting mechanisms , 2014, Breast Cancer Research and Treatment.

[18]  S. Cook,et al.  Adaptation to mTOR kinase inhibitors by amplification of eIF4E to maintain cap-dependent translation , 2014, Journal of Cell Science.

[19]  Qiang Zhang,et al.  Disrupting the interaction of BRD4 with diacetylated Twist suppresses tumorigenesis in basal-like breast cancer. , 2014, Cancer cell.

[20]  Wai Leong Tam,et al.  The epigenetics of epithelial-mesenchymal plasticity in cancer , 2013, Nature Medicine.

[21]  B. Zhou,et al.  The Role of Snail in EMT and Tumorigenesis. , 2013, Current cancer drug targets.

[22]  David A. Scott,et al.  Genome engineering using the CRISPR-Cas9 system , 2013, Nature Protocols.

[23]  David A. Scott,et al.  Double Nicking by RNA-Guided CRISPR Cas9 for Enhanced Genome Editing Specificity , 2013, Cell.

[24]  R. Schneider,et al.  4E-BP restrains eIF4E phosphorylation , 2013, Translation.

[25]  Q. She,et al.  ERK and AKT signaling cooperate to translationally regulate survivin expression for metastatic progression of colorectal cancer , 2013, Oncogene.

[26]  E. Nakakura,et al.  Incomplete inhibition of phosphorylation of 4E-BP1 as a mechanism of primary resistance to ATP-competitive mTOR inhibitors , 2013, Oncogene.

[27]  Jun Yao,et al.  Loss of FBP1 by Snail-mediated repression provides metabolic advantages in basal-like breast cancer. , 2013, Cancer cell.

[28]  Y. Martineau,et al.  Anti-oncogenic potential of the eIF4E-binding proteins , 2013, Oncogene.

[29]  N. Sonenberg,et al.  eIF4E/4E-BP ratio predicts the efficacy of mTOR targeted therapies. , 2012, Cancer research.

[30]  C. Sander,et al.  Genome Sequencing Identifies a Basis for Everolimus Sensitivity , 2012, Science.

[31]  D. Sabatini,et al.  mTOR Signaling in Growth Control and Disease , 2012, Cell.

[32]  J. Baselga,et al.  Dual Mtorc1/2 and Her2 Blockade Results in Antitumor Activity in Preclinical Models of Breast Cancer Resistant to Anti-her2 Therapy Statement of Translational Relevance , 2022 .

[33]  Nicholas T. Ingolia,et al.  The translational landscape of mTOR signalling steers cancer initiation and metastasis , 2012, Nature.

[34]  M. Hall,et al.  Rapamycin passes the torch: a new generation of mTOR inhibitors , 2011, Nature Reviews Drug Discovery.

[35]  H. Weiss,et al.  mTORC1 and mTORC2 regulate EMT, motility, and metastasis of colorectal cancer via RhoA and Rac1 signaling pathways. , 2011, Cancer research.

[36]  Sik Yoon,et al.  SNAI1 is Involved in the Proliferation and Migration of Glioblastoma Cells , 2011, Cellular and Molecular Neurobiology.

[37]  Yoshikazu Nakamura,et al.  Expression of snail in epidermal keratinocytes promotes cutaneous inflammation and hyperplasia conducive to tumor formation. , 2010, Cancer research.

[38]  Q. She,et al.  4E-BP1 is a key effector of the oncogenic activation of the AKT and ERK signaling pathways that integrates their function in tumors. , 2010, Cancer cell.

[39]  J. Friedberg,et al.  The pan-HDAC inhibitor vorinostat potentiates the activity of the proteasome inhibitor carfilzomib in human DLBCL cells in vitro and in vivo. , 2010, Blood.

[40]  N. Sonenberg,et al.  mTORC1-Mediated Cell Proliferation, But Not Cell Growth, Controlled by the 4E-BPs , 2010, Science.

[41]  K. Shokat,et al.  Genetic dissection of the oncogenic mTOR pathway reveals druggable addiction to translational control via 4EBP-eIF4E. , 2010, Cancer cell.

[42]  R. Huang,et al.  Epithelial-Mesenchymal Transitions in Development and Disease , 2009, Cell.

[43]  A. Hinnebusch,et al.  Regulation of Translation Initiation in Eukaryotes: Mechanisms and Biological Targets , 2009, Cell.

[44]  Hans E. Huber,et al.  Breast Tumor Cells with PI3K Mutation or HER2 Amplification Are Selectively Addicted to Akt Signaling , 2008, PloS one.

[45]  C. Proud,et al.  Regulation of cyclin D1 expression by mTORC1 signaling requires eukaryotic initiation factor 4E-binding protein 1 , 2008, Oncogene.

[46]  S. Murray,et al.  Repression of PTEN Phosphatase by Snail1 Transcriptional Factor during Gamma Radiation-Induced Apoptosis , 2008, Molecular and Cellular Biology.

[47]  Héctor Peinado,et al.  Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype? , 2007, Nature Reviews Cancer.

[48]  J. Blenis,et al.  RAS/ERK Signaling Promotes Site-specific Ribosomal Protein S6 Phosphorylation via RSK and Stimulates Cap-dependent Translation* , 2007, Journal of Biological Chemistry.

[49]  N. Dave,et al.  Expression of Snail protein in tumor–stroma interface , 2006, Oncogene.

[50]  Gordon B Mills,et al.  mTOR inhibition induces upstream receptor tyrosine kinase signaling and activates Akt. , 2006, Cancer research.

[51]  A. Brasier,et al.  Two-step cross-linking method for identification of NF-kappaB gene network by chromatin immunoprecipitation. , 2005, BioTechniques.

[52]  G. Berx,et al.  DeltaEF1 is a transcriptional repressor of E-cadherin and regulates epithelial plasticity in breast cancer cells , 2005, Oncogene.

[53]  Elaine Fuchs,et al.  A Signaling Pathway Involving TGF-β2 and Snail in Hair Follicle Morphogenesis , 2004, PLoS biology.

[54]  I. Fabregat,et al.  Snail blocks the cell cycle and confers resistance to cell death. , 2004, Genes & development.

[55]  E. Ballestar,et al.  Snail Mediates E-Cadherin Repression by the Recruitment of the Sin3A/Histone Deacetylase 1 (HDAC1)/HDAC2 Complex , 2004, Molecular and Cellular Biology.

[56]  E. Fearon,et al.  The SLUG zinc-finger protein represses E-cadherin in breast cancer. , 2002, Cancer research.

[57]  M. Nieto,et al.  The snail superfamily of zinc-finger transcription factors , 2002, Nature Reviews Molecular Cell Biology.

[58]  J. Fando,et al.  4E binding protein 1 expression is inversely correlated to the progression of gastrointestinal cancers. , 2000, The international journal of biochemistry & cell biology.

[59]  A. G. Herreros,et al.  The transcription factor Snail is a repressor of E-cadherin gene expression in epithelial tumour cells , 2000, Nature Cell Biology.

[60]  Francisco Portillo,et al.  The transcription factor Snail controls epithelial–mesenchymal transitions by repressing E-cadherin expression , 2000, Nature Cell Biology.

[61]  Y. Lutz,et al.  Definition of the DNA-binding site repertoire for the Drosophila transcription factor SNAIL. , 1993, Nucleic acids research.

[62]  W. McGuire,et al.  Association of p53 protein expression with tumor cell proliferation rate and clinical outcome in node-negative breast cancer. , 1993, Journal of the National Cancer Institute.

[63]  A. S. A. Don,et al.  Recent clinical trials of mTOR-targeted cancer therapies. , 2011, Reviews on recent clinical trials.

[64]  Lisa L. Smith,et al.  AZD8055 is a potent, selective, and orally bioavailable ATP-competitive mammalian target of rapamycin kinase inhibitor with in vitro and in vivo antitumor activity. , 2010, Cancer research.

[65]  L. Saal,et al.  Recurrent gross mutations of the PTEN tumor suppressor gene in breast cancers with deficient DSB repair , 2008, Nature Genetics.

[66]  C. Hoffmann,et al.  Flow cytometric analysis of G1- and G2/M-phase subpopulations in mammalian cell nuclei using side scatter and DNA content measurements. , 1990, Cytometry.