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Pesquisa : D12.776.260.665.400 [Categoria DeCS]
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[PMID]:28938120
[Au] Autor:Shorter J
[Ad] Endereço:Department of Biochemistry and Biophysics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: jshorter@mail.med.upenn.edu.
[Ti] Título:Prion-like Domains Program Ewing's Sarcoma.
[So] Source:Cell;171(1):30-31, 2017 09 21.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prion-like domains have emerged as important drivers of neurodegenerative disease. Now, Boulay et al. establish that the translocated prion-like domain of the oncogenic EWS-FLI1 fusion protein enables phase-separation events, which inappropriately recruit chromatin-remodeling factors to elicit the aberrant transcriptional programs underlying Ewing's sarcoma.
[Mh] Termos MeSH primário: Proteína EWS de Ligação a RNA
Sarcoma de Ewing
[Mh] Termos MeSH secundário: Seres Humanos
Proteínas de Fusão Oncogênicas
Príons
Proteína Proto-Oncogênica c-fli-1
Fatores de Transcrição
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (EWS-FLI fusion protein); 0 (Oncogene Proteins, Fusion); 0 (Prions); 0 (Proto-Oncogene Protein c-fli-1); 0 (RNA-Binding Protein EWS); 0 (Transcription Factors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE


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[PMID]:28844694
[Au] Autor:Boulay G; Sandoval GJ; Riggi N; Iyer S; Buisson R; Naigles B; Awad ME; Rengarajan S; Volorio A; McBride MJ; Broye LC; Zou L; Stamenkovic I; Kadoch C; Rivera MN
[Ad] Endereço:Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.
[Ti] Título:Cancer-Specific Retargeting of BAF Complexes by a Prion-like Domain.
[So] Source:Cell;171(1):163-178.e19, 2017 Sep 21.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alterations in transcriptional regulators can orchestrate oncogenic gene expression programs in cancer. Here, we show that the BRG1/BRM-associated factor (BAF) chromatin remodeling complex, which is mutated in over 20% of human tumors, interacts with EWSR1, a member of a family of proteins with prion-like domains (PrLD) that are frequent partners in oncogenic fusions with transcription factors. In Ewing sarcoma, we find that the BAF complex is recruited by the EWS-FLI1 fusion protein to tumor-specific enhancers and contributes to target gene activation. This process is a neomorphic property of EWS-FLI1 compared to wild-type FLI1 and depends on tyrosine residues that are necessary for phase transitions of the EWSR1 prion-like domain. Furthermore, fusion of short fragments of EWSR1 to FLI1 is sufficient to recapitulate BAF complex retargeting and EWS-FLI1 activities. Our studies thus demonstrate that the physical properties of prion-like domains can retarget critical chromatin regulatory complexes to establish and maintain oncogenic gene expression programs.
[Mh] Termos MeSH primário: Proteínas de Ligação a Calmodulina/química
Proteínas de Ligação a Calmodulina/metabolismo
Proteínas de Fusão Oncogênicas/metabolismo
Proteína Proto-Oncogênica c-fli-1/metabolismo
Proteína EWS de Ligação a RNA/metabolismo
Proteínas de Ligação a RNA/química
Proteínas de Ligação a RNA/metabolismo
Sarcoma de Ewing/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proteínas de Ligação a DNA/química
Proteínas de Ligação a DNA/metabolismo
Seres Humanos
Células Mesenquimais Estromais/metabolismo
Repetições de Microssatélites
Complexos Multiproteicos/química
Complexos Multiproteicos/metabolismo
Proteínas Nucleares/química
Proteínas Nucleares/metabolismo
Proteínas Priônicas/metabolismo
Domínios Proteicos
Sarcoma de Ewing/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BANF1 protein, human); 0 (Calmodulin-Binding Proteins); 0 (DNA-Binding Proteins); 0 (EWS-FLI fusion protein); 0 (EWSR1 protein, human); 0 (FLI1 protein, human); 0 (Multiprotein Complexes); 0 (Nuclear Proteins); 0 (Oncogene Proteins, Fusion); 0 (Prion Proteins); 0 (Proto-Oncogene Protein c-fli-1); 0 (RNA-Binding Protein EWS); 0 (RNA-Binding Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE


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[PMID]:28671673
[Au] Autor:Katschnig AM; Kauer MO; Schwentner R; Tomazou EM; Mutz CN; Linder M; Sibilia M; Alonso J; Aryee DNT; Kovar H
[Ad] Endereço:Children's Cancer Research Institute, St Anna Kinderkrebsforschung, Vienna, Austria.
[Ti] Título:EWS-FLI1 perturbs MRTFB/YAP-1/TEAD target gene regulation inhibiting cytoskeletal autoregulatory feedback in Ewing sarcoma.
[So] Source:Oncogene;36(43):5995-6005, 2017 Oct 26.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ewing sarcoma (EWS) is a paediatric bone cancer with high metastatic potential. Cellular plasticity resulting from dynamic cytoskeletal reorganization, typically regulated via the Rho pathway, is a prerequisite for metastasis initiation. Here, we interrogated the role of the Ewing sarcoma driver oncogene EWS-FLI1 in cytoskeletal reprogramming. We report that EWS-FLI1 strongly represses the activity of the Rho-F-actin signal pathway transcriptional effector MRTFB, affecting the expression of a large number of EWS-FLI1-anticorrelated genes including structural and regulatory cytoskeletal genes. Consistent with this finding, chromatin immunoprecipitation sequencing (ChIP-seq) revealed strong overlaps in myocardin-related transcription factor B (MRTFB) and EWS-FLI1 chromatin occupation, especially for EWS-FLI1-anticorrelated genes. Binding of the transcriptional co-activator Yes-associated protein (YAP)-1, enrichment of TEAD-binding motifs in these shared genomic binding regions and overlapping transcriptional footprints of MRTFB and TEAD factors led us to propose synergy between MRTFB and the YAP/TEAD complex in the regulation of EWS-FLI1-anticorrelated genes. We propose that EWS-FLI1 suppresses the Rho-actin pathway by perturbation of a MRTFB/YAP-1/TEAD transcriptional module, which directly affects the actin-autoregulatory feedback loop. As spontaneous fluctuations in EWS-FLI1 levels of Ewing sarcoma cells in vitro and in vivo, associated with a switch between a proliferative, non-migratory EWS-FLI1-high and a non-proliferative highly migratory EWS-FLI1-low state, were recently described, our data provide a mechanistic basis for the underlying EWS-FLI1-dependent reversible cytoskeletal reprogramming of Ewing sarcoma cells.
[Mh] Termos MeSH primário: Reprogramação Celular/genética
Citoesqueleto/genética
Proteínas de Fusão Oncogênicas/genética
Proteína Proto-Oncogênica c-fli-1/genética
Proteína EWS de Ligação a RNA/genética
Sarcoma de Ewing/genética
[Mh] Termos MeSH secundário: Actinas/genética
Linhagem Celular Tumoral
Proliferação Celular/genética
Cromatina/genética
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Sarcoma de Ewing/patologia
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Chromatin); 0 (EWS-FLI fusion protein); 0 (Oncogene Proteins, Fusion); 0 (Proto-Oncogene Protein c-fli-1); 0 (RNA-Binding Protein EWS)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.202


  4 / 811 MEDLINE  
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[PMID]:28542597
[Au] Autor:Moore C; Parrish JK; Jedlicka P
[Ad] Endereço:Center for Cancer and Blood Disorders, Children's Hospital Colorado, Aurora, Colorado, United States of America.
[Ti] Título:MiR-193b, downregulated in Ewing Sarcoma, targets the ErbB4 oncogene to inhibit anchorage-independent growth.
[So] Source:PLoS One;12(5):e0178028, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ewing Sarcoma is an aggressive, oncofusion-driven, malignant neoplasm of bone and soft tissue affecting predominantly children and young adults. Seeking to identify potential novel therapeutic targets/agents for this disease, our previous studies uncovered microRNAs regulated by EWS/Fli1, the most common oncofusion, with growth modulatory properties. In the present study, we sought to identify EWS/Fli1-repressed, growth suppressive, microRNAs potentially amenable to replacement in Ewing Sarcoma cells. Eight microRNAs (143, 153, 184, 193b, 195, 203, 206 and 223) were selected for evaluation as EWS/Fli1-repressed and underexpressed in Ewing Sarcoma cells, and reported to be growth suppressive in other pediatric or/and adult cancers. The selected miRs, and appropriate non-targeting controls, were introduced into two different Ewing Sarcoma cell lines (A673 and SK-ES-1), and effects on growth were examined using a high and low-density growth assay. MiR-193b was growth inhibitory in both assays and cell lines. In subsequent analyses, we found that stable overexpression of miR-193b also inhibits anchorage-independent growth in both A673 and SK-ES-1 cells. We further show that miR-193b negatively regulates expression of the ErbB4 oncogene in A673 and SK-ES-1 cells, and that depletion of ErbB4 is itself inhibitory to anchorage-independent growth in the same cell lines. Together, our studies show that the EWS/Fli1-repressed miR-193b is growth suppressive in Ewing Sarcoma, and identify ErbB4 as a target gene and candidate mediator of this growth suppression.
[Mh] Termos MeSH primário: MicroRNAs/metabolismo
Receptor ErbB-4/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Antagomirs/metabolismo
Sequência de Bases
Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/patologia
Linhagem Celular Tumoral
Proliferação Celular
Regulação para Baixo
Seres Humanos
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Proteínas de Fusão Oncogênicas/metabolismo
Proteína Proto-Oncogênica c-fli-1/metabolismo
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Proteína EWS de Ligação a RNA/metabolismo
Receptor ErbB-4/antagonistas & inibidores
Receptor ErbB-4/genética
Sarcoma de Ewing/metabolismo
Sarcoma de Ewing/patologia
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antagomirs); 0 (EWS-FLI fusion protein); 0 (MicroRNAs); 0 (Oncogene Proteins, Fusion); 0 (Proto-Oncogene Protein c-fli-1); 0 (RNA, Small Interfering); 0 (RNA-Binding Protein EWS); EC 2.7.10.1 (ERBB4 protein, human); EC 2.7.10.1 (Receptor, ErbB-4)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178028


  5 / 811 MEDLINE  
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[PMID]:28528914
[Au] Autor:Saigusa R; Asano Y; Nakamura K; Hirabayashi M; Miura S; Yamashita T; Taniguchi T; Ichimura Y; Takahashi T; Yoshizaki A; Miyagaki T; Sugaya M; Sato S
[Ad] Endereço:Department of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
[Ti] Título:Systemic Sclerosis Dermal Fibroblasts Suppress Th1 Cytokine Production via Galectin-9 Overproduction due to Fli1 Deficiency.
[So] Source:J Invest Dermatol;137(9):1850-1859, 2017 Sep.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dermal fibroblasts promote skin-localized transdifferentiation of regulatory T cells to T helper (Th) type 2-like cells in systemic sclerosis (SSc). However, the entire effect of SSc dermal fibroblasts on immune cells still remains unknown. Because galectin-9 induces Th2 cytokine-predominant immune imbalance by negatively regulating Th1/Th17 cells in inflammatory diseases, we investigated the contribution of galectin-9 to Th immune balance in SSc lesional skin. We used human clinical samples and Fli1 mice because Fli1 deficiency induces SSc-like phenotypes in various cell types. Galectin-9 was overexpressed in SSc dermal fibroblasts in vivo and in vitro. Serum galectin-9 levels were significantly elevated in SSc patients and positively correlated with skin score. Galectin-9 was up-regulated by autocrine endothelin stimulation and Fli1 deficiency, and Fli1 occupied the LGALS9 promoter in dermal fibroblasts. Co-culture of splenic CD4 T cells with Fli1 dermal fibroblasts significantly increased IL-4-producing cell proportion, and this effect was cancelled in parallel with the increased interferon-γ production when Fli1 dermal fibroblasts were transfected with Lgals9 small interfering RNA. Furthermore, Lgals9 small interfering RNA suppressed dermal collagen deposition by increasing interferon-γ production of skin-infiltrating CD4 T cells in bleomycin-treated mice. These results suggest that SSc dermal fibroblasts suppress interferon-γ expression of skin-infiltrating CD4 T cells through galectin-9 overproduction, promoting skin fibrosis development.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Galectinas/genética
Proteína Proto-Oncogênica c-fli-1/deficiência
Escleroderma Sistêmico/genética
Células Th1/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Modelos Animais de Doenças
Feminino
Fibroblastos/citologia
Fibroblastos/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Masculino
Camundongos
Camundongos Transgênicos
Distribuição Aleatória
Valores de Referência
Escleroderma Sistêmico/fisiopatologia
Regulação para Cima
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Galectins); 0 (LGALS9 protein, human); 0 (Proto-Oncogene Protein c-fli-1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE


  6 / 811 MEDLINE  
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[PMID]:28432223
[Au] Autor:Vo KK; Jarocha DJ; Lyde RB; Hayes V; Thom CS; Sullivan SK; French DL; Poncz M
[Ad] Endereço:Department of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
[Ti] Título:FLI1 level during megakaryopoiesis affects thrombopoiesis and platelet biology.
[So] Source:Blood;129(26):3486-3494, 2017 Jun 29.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Friend leukemia virus integration 1 (FLI1), a critical transcription factor (TF) during megakaryocyte differentiation, is among genes hemizygously deleted in Jacobsen syndrome, resulting in a macrothrombocytopenia termed Paris-Trousseau syndrome (PTSx). Recently, heterozygote human mutations have been ascribed to cause thrombocytopenia. We studied induced-pluripotent stem cell (iPSC)-derived megakaryocytes (iMegs) to better understand these clinical disorders, beginning with iPSCs generated from a patient with PTSx and iPSCs from a control line with a targeted heterozygous knockout (FLI1 ). PTSx and FLI1 iMegs replicate many of the described megakaryocyte/platelet features, including a decrease in iMeg yield and fewer platelets released per iMeg. Platelets released in vivo from infusion of these iMegs had poor half-lives and functionality. We noted that the closely linked E26 transformation-specific proto-oncogene 1 (ETS1) is overexpressed in these FLI1-deficient iMegs, suggesting FLI1 negatively regulates ETS1 in megakaryopoiesis. Finally, we examined whether FLI1 overexpression would affect megakaryopoiesis and thrombopoiesis. We found increased yield of noninjured, in vitro iMeg yield and increased in vivo yield, half-life, and functionality of released platelets. These studies confirm heterozygosity results in pleiotropic defects similar to those noted with other critical megakaryocyte-specific TFs; however, unlike those TFs, FLI1 overexpression improved yield and functionality.
[Mh] Termos MeSH primário: Síndrome da Deleção Distal 11q de Jacobsen/patologia
Megacariócitos/citologia
Proteína Proto-Oncogênica c-fli-1/sangue
Trombopoese
[Mh] Termos MeSH secundário: Animais
Plaquetas/metabolismo
Diferenciação Celular
Linhagem Celular
Seres Humanos
Células-Tronco Pluripotentes Induzidas
Camundongos
Camundongos SCID
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FLI1 protein, human); 0 (Proto-Oncogene Protein c-fli-1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-02-770958


  7 / 811 MEDLINE  
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[PMID]:28358102
[Au] Autor:Ledford H
[Ti] Título:Cruel fusion: What a young man's death means for childhood cancer.
[So] Source:Nature;543(7647):608-611, 2017 03 28.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Proteínas de Fusão Oncogênicas/genética
Proteínas de Fusão Oncogênicas/metabolismo
Proteína Proto-Oncogênica c-fli-1/genética
Proteína Proto-Oncogênica c-fli-1/metabolismo
Proteína EWS de Ligação a RNA/genética
Proteína EWS de Ligação a RNA/metabolismo
Sarcoma de Ewing/genética
Sarcoma de Ewing/terapia
[Mh] Termos MeSH secundário: Adolescente
Morte
Epigênese Genética
Seres Humanos
Masculino
Proteínas de Fusão Oncogênicas/antagonistas & inibidores
Proteínas de Fusão Oncogênicas/química
Proteína Proto-Oncogênica c-fli-1/antagonistas & inibidores
Proteína Proto-Oncogênica c-fli-1/química
Interferência de RNA
Proteína EWS de Ligação a RNA/antagonistas & inibidores
Proteína EWS de Ligação a RNA/química
Receptores de Somatomedina/genética
Receptores de Somatomedina/imunologia
Sarcoma de Ewing/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EWS-FLI fusion protein); 0 (IGF1R protein, human); 0 (Oncogene Proteins, Fusion); 0 (Proto-Oncogene Protein c-fli-1); 0 (RNA-Binding Protein EWS); 0 (Receptors, Somatomedin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1038/543608a


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[PMID]:28248553
[Au] Autor:Looney AP; Han R; Stawski L; Marden G; Iwamoto M; Trojanowska M
[Ad] Endereço:1 Boston University School of Medicine, Arthritis Center/Rheumatology, Boston, Massachusetts; and.
[Ti] Título:Synergistic Role of Endothelial ERG and FLI1 in Mediating Pulmonary Vascular Homeostasis.
[So] Source:Am J Respir Cell Mol Biol;57(1):121-131, 2017 Jul.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endothelial cell (EC) activation underlies many vascular diseases, including pulmonary arterial hypertension (PAH). Several members of the E-twenty six (ETS) family of transcription factors are important regulators of the gene network governing endothelial homeostasis, and their aberrant expression is associated with pathological angiogenesis. The goal of this study was to determine whether deficiencies of the ETS family member, Friend leukemia integration 1 transcription factor (FLI1), and its closest homolog, ETS-related gene (ERG), are associated with PAH. We found that endothelial ERG was significantly reduced in the lung samples from patients with PAH, as well as in chronically hypoxic mice. Functional studies revealed that depletion of ERG or FLI1 in human pulmonary ECs led to increased expression of inflammatory genes, including IFN genes, whereas genes regulating endothelial homeostasis and cell-cell adhesion were down-regulated. Simultaneous knockdown of both ERG and FLI1 had synergistic or additive effects on the expression of these genes, suggesting that ERG and FLI1 coregulate at least a subset of their target genes. Functionally, knockdown of ERG and FLI1 induced cell monolayer permeability with a potency similar to that of vascular endothelial growth factor. Notably, stimulation of ECs with Toll-like receptor 3 ligand poly(I:C) suppressed ERG expression and induced ERG dissociation from the IFNB1 promoter, while promoting signal transducers and activators of transcription 1 (STAT1) recruitment. Consistent with the up-regulation of inflammatory genes seen in vitro, Erg and Fli1 double-heterozygote mice showed increased immune cell infiltration and expression of cytokines in the lung. In conclusion, loss of ERG and FLI1 might contribute to the pathogenesis of vascular lung complications through the induction of inflammation.
[Mh] Termos MeSH primário: Endotélio Vascular/metabolismo
Homeostase
Pulmão/irrigação sanguínea
Proteínas Oncogênicas/metabolismo
Proteína Proto-Oncogênica c-fli-1/metabolismo
Regulador Transcricional ERG/metabolismo
[Mh] Termos MeSH secundário: Animais
Doença Crônica
Regulação para Baixo/efeitos dos fármacos
Regulação para Baixo/genética
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/patologia
Feminino
Heterozigoto
Homeostase/efeitos dos fármacos
Homeostase/genética
Seres Humanos
Hipertensão Pulmonar/complicações
Hipertensão Pulmonar/genética
Hipertensão Pulmonar/patologia
Hipóxia/complicações
Hipóxia/genética
Hipóxia/patologia
Interferon beta/genética
Pulmão/patologia
Masculino
Camundongos Endogâmicos C57BL
Proteínas Oncogênicas/genética
Pneumonia/complicações
Pneumonia/genética
Pneumonia/patologia
Poli I-C/farmacologia
Regiões Promotoras Genéticas/genética
Proteína Proto-Oncogênica c-fli-1/genética
Artéria Pulmonar/patologia
Fator de Transcrição STAT1/metabolismo
Regulador Transcricional ERG/genética
Regulação para Cima/efeitos dos fármacos
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ERG protein, human); 0 (ERG protein, mouse); 0 (Oncogene Proteins); 0 (Proto-Oncogene Protein c-fli-1); 0 (STAT1 Transcription Factor); 0 (Transcriptional Regulator ERG); 77238-31-4 (Interferon-beta); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2016-0200OC


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[PMID]:28232470
[Au] Autor:Takahashi T; Asano Y; Sugawara K; Yamashita T; Nakamura K; Saigusa R; Ichimura Y; Toyama T; Taniguchi T; Akamata K; Noda S; Yoshizaki A; Tsuruta D; Trojanowska M; Sato S
[Ad] Endereço:Department of Dermatology, University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8655, Japan.
[Ti] Título:Epithelial Fli1 deficiency drives systemic autoimmunity and fibrosis: Possible roles in scleroderma.
[So] Source:J Exp Med;214(4):1129-1151, 2017 Apr 03.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Systemic sclerosis (SSc), or scleroderma, is a multisystem autoimmune disorder characterized by vasculopathy and fibrosis in the skin and internal organs, most frequently in the esophagus and lungs. Hitherto, studies on SSc pathogenesis centered on immune cells, vascular cells, and fibroblasts. Although dysregulated keratinocytes in SSc have been recently reported, the contribution of epithelial cells to pathogenesis remains unexplored. In this study, we demonstrated the induction of SSc-like molecular phenotype in keratinocytes by gene silencing of transcription factor Friend leukemia virus integration 1 (Fli1), the deficiency of which is implicated in SSc pathogenesis. Keratin 14-expressing epithelial cell-specific knockout mice spontaneously developed dermal and esophageal fibrosis with epithelial activation. Furthermore, they developed remarkable autoimmunity with interstitial lung disease derived from thymic defects with down-regulation of autoimmune regulator (Aire). Importantly, Fli1 directly regulated Aire expression in epithelial cells. Collectively, epithelial Fli1 deficiency might be involved in the systemic autoimmunity and selective organ fibrosis in SSc. This study uncovers unidentified roles of dysregulated epithelial cells in SSc pathogenesis.
[Mh] Termos MeSH primário: Autoimunidade
Proteína Proto-Oncogênica c-fli-1/fisiologia
Escleroderma Sistêmico/etiologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Células Epiteliais/fisiologia
Esôfago/patologia
Fibrose
Proteínas de Homeodomínio/fisiologia
Seres Humanos
Queratina-14/análise
Queratinócitos/metabolismo
Camundongos
Pele/patologia
Células Th17/fisiologia
Células Th2/fisiologia
Fatores de Transcrição/genética
Fatores de Transcrição/fisiologia
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APECED protein); 0 (FLI1 protein, human); 0 (Fli1 protein, mouse); 0 (Homeodomain Proteins); 0 (Keratin-14); 0 (Proto-Oncogene Protein c-fli-1); 0 (Transcription Factors); 128559-51-3 (RAG-1 protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20160247


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[PMID]:28135250
[Au] Autor:Franzetti GA; Laud-Duval K; van der Ent W; Brisac A; Irondelle M; Aubert S; Dirksen U; Bouvier C; de Pinieux G; Snaar-Jagalska E; Chavrier P; Delattre O
[Ad] Endereço:Institut Curie, PSL Research University, Paris cedex 05, France.
[Ti] Título:Cell-to-cell heterogeneity of EWSR1-FLI1 activity determines proliferation/migration choices in Ewing sarcoma cells.
[So] Source:Oncogene;36(25):3505-3514, 2017 Jun 22.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ewing sarcoma is characterized by the expression of the chimeric EWSR1-FLI1 transcription factor. Proteomic analyses indicate that the decrease of EWSR1-FLI1 expression leads to major changes in effectors of the dynamics of the actin cytoskeleton and the adhesion processes with a shift from cell-to-cell to cell-matrix adhesion. These changes are associated with a dramatic increase of in vivo cell migration and invasion potential. Importantly, EWSR1-FLI1 expression, evaluated by single-cell RT-ddPCR/immunofluorescence analyses, and activity, assessed by expression of EWSR1-FLI1 downstream targets, are heterogeneous in cell lines and in tumours and can fluctuate along time in a fully reversible process between EWSR1-FLI1 states, characterized by highly active cell proliferation, and EWSR1-FLI1 states where cells have a strong propensity to migrate, invade and metastasize. This new model of phenotypic plasticity proposes that the dynamic fluctuation of the expression level of a dominant oncogene is an intrinsic characteristic of its oncogenic potential.
[Mh] Termos MeSH primário: Proteínas de Ligação a Calmodulina/biossíntese
Movimento Celular
Proliferação Celular
Regulação Neoplásica da Expressão Gênica
Proteínas de Fusão Oncogênicas/biossíntese
Proteína Proto-Oncogênica c-fli-1/biossíntese
Proteínas de Ligação a RNA/biossíntese
Sarcoma de Ewing/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas de Ligação a Calmodulina/genética
Linhagem Celular Tumoral
Camundongos
Camundongos SCID
Invasividade Neoplásica
Metástase Neoplásica
Proteínas de Fusão Oncogênicas/genética
Proteína Proto-Oncogênica c-fli-1/genética
Proteína EWS de Ligação a RNA
Proteínas de Ligação a RNA/genética
Sarcoma de Ewing/genética
Sarcoma de Ewing/patologia
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calmodulin-Binding Proteins); 0 (Ewsr1 protein, mouse); 0 (Fli1 protein, mouse); 0 (Oncogene Proteins, Fusion); 0 (Proto-Oncogene Protein c-fli-1); 0 (RNA-Binding Protein EWS); 0 (RNA-Binding Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170131
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2016.498



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