Base de dados : MEDLINE
Pesquisa : D12.644.360.024.500.906 [Categoria DeCS]
Referências encontradas : 90 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 9 ir para página                      

  1 / 90 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28425962
[Au] Autor:Iyengar PV
[Ad] Endereço:Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore. csipvi@nus.edu.sg.
[Ti] Título:Regulation of Ubiquitin Enzymes in the TGF-ß Pathway.
[So] Source:Int J Mol Sci;18(4), 2017 Apr 20.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The transforming growth factor-ß (TGF-ß) pathway has a tumor suppressor role in normal and premalignant cells but promotes oncogenesis in advanced cancer cells. Components of the pathway are tightly controlled by ubiquitin modifying enzymes and aberrations in these enzymes are frequently observed to dysregulate the pathway causing diseases such as bone disorders, cancer and metastasis. These enzymes and their counterparts are increasingly being tested as druggable targets, and thus a deeper understanding of the enzymes is required. This review summarizes the roles of specific ubiquitin modifying enzymes in the TGF-ß pathway and how they are regulated.
[Mh] Termos MeSH primário: Transdução de Sinais
Fator de Crescimento Transformador beta/metabolismo
Ubiquitina/metabolismo
[Mh] Termos MeSH secundário: Animais
Suscetibilidade a Doenças
Seres Humanos
Complexo de Endopeptidases do Proteassoma/metabolismo
Ligação Proteica
Sumoilação
Fator 4 Associado a Receptor de TNF/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (TNF Receptor-Associated Factor 4); 0 (Transforming Growth Factor beta); 0 (Ubiquitin); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[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:170421
[St] Status:MEDLINE


  2 / 90 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27842582
[Au] Autor:Meerson A; Yehuda H
[Ad] Endereço:Molecular Biology of Chronic Diseases, MIGAL Galilee Research Institute, PO Box 831, Kiryat Shmona, 11016, Israel. arim@migal.org.il.
[Ti] Título:Leptin and insulin up-regulate miR-4443 to suppress NCOA1 and TRAF4, and decrease the invasiveness of human colon cancer cells.
[So] Source:BMC Cancer;16(1):882, 2016 11 14.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Obesity is a risk factor for colorectal cancer (CRC). Normal and tumor cells respond to metabolic hormones, such as leptin and insulin. Thus, obesity-associated resistance to these hormones likely leads to changes in gene expression and behavior of tumor cells. However, the mechanisms affected by leptin and insulin signaling in CRC cells remain mostly unknown. METHODS: We hypothesized that microRNAs (miRNAs) are involved in the regulation of tumorigenesis-related gene expression in CRC cells by leptin and insulin. To test this hypothesis, miRNA levels in the CRC-derived cell lines HCT-116, HT-29 and DLD-1 were profiled, following leptin and insulin treatment. Candidate miRNAs were validated by RT-qPCR. Predicted miRNA targets with known roles in cancer, were validated by immunoblots and reporter assays in HCT-116 cells. Transfection of HCT-116 cells with candidate miRNA mimic was used to test in vitro effects on proliferation and invasion. RESULTS: Of ~800 miRNAs profiled, miR-4443 was consistently up-regulated by leptin and insulin in HCT-116 and HT-29, but not in DLD-1, which lacked normal leptin receptor expression. Dose response experiments showed that leptin at 100 ng/ml consistently up-regulated miR-4443 in HCT-116 cells, concomitantly with a significant decrease in cell invasion ability. Transfection with miR-4443 mimic decreased invasion and proliferation of HCT-116 cells. Moreover, leptin and miR-4443 transfection significantly down-regulated endogenous NCOA1 and TRAF4, both predicted targets of miR-4443 with known roles in cancer metastasis. miR-4443 was found to directly regulate TRAF4 and NCOA1, as validated by a reporter assay. The up-regulation of miR-4443 by leptin or insulin was attenuated by the inhibition of MEK1/2. CONCLUSIONS: Our findings suggest that miR-4443 acts in a tumor-suppressive manner by down-regulating TRAF4 and NCOA1 downstream of MEK-C/EBP-mediated leptin and insulin signaling, and that insulin and/or leptin resistance (e.g. in obesity) may suppress this pathway and increase the risk of metastatic CRC.
[Mh] Termos MeSH primário: Neoplasias do Colo/genética
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Insulina/farmacologia
Leptina/farmacologia
MicroRNAs/genética
Coativador 1 de Receptor Nuclear/genética
Fator 4 Associado a Receptor de TNF/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Movimento Celular/genética
Proliferação Celular
Neoplasias do Colo/metabolismo
Neoplasias do Colo/patologia
Perfilação da Expressão Gênica
Células HCT116
Seres Humanos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Modelos Biológicos
Interferência de RNA
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Insulin); 0 (Leptin); 0 (MIRN-4443 microRNA, human); 0 (MicroRNAs); 0 (TNF Receptor-Associated Factor 4); EC 2.3.1.48 (Nuclear Receptor Coactivator 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161116
[St] Status:MEDLINE


  3 / 90 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27086366
[Au] Autor:Górska A; Gruchala-Niedoszytko M; Niedoszytko M; Maciejewska A; Chelminska M; Skrzypski M; Wasag B; Kaczkan M; Lange M; Nedoszytko B; Pawlowski R; Malgorzewicz S; Jassem E
[Ad] Endereço:Department of Allergology, Medical University of Gdansk, Gdansk, Poland.
[Ti] Título:The Role of TRAF4 and B3GAT1 Gene Expression in the Food Hypersensitivity and Insect Venom Allergy in Mastocytosis.
[So] Source:Arch Immunol Ther Exp (Warsz);64(6):497-503, 2016 Dec.
[Is] ISSN:1661-4917
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Mastocytosis is an uncommon disease classified as a myeloproliferative neoplasm, however, its symptoms are broad and place patients at crossroads between dermatology, hematology and allergology. Patients with mastocytosis often suffer from symptoms resulting from the activation and release of mediators from the mast cells, such as generalized itching, redness, headache, abdominal cramps, diarrhea, bone pain or arthritis, hypotension and shock. The possible severe, fatal or near fatal reactions caused by food hypersensitivity are reasons for the research focused on marker identification. The aim of the study was to analyse the gene expression differences in mastocytosis patients with and without food and drug hypersensitivity and insect venom allergy (IVA). A total of 57 Caucasian patients with mastocytosis were studied [median age 41.8; range 18-77 years; 15 (26.3 %) males and 42 (73.7 %) females]. Quantitative RT-PCRs of 11 genes plus ribosomal 18S RNA were run. Symptoms of food hypersensitivity were found in 12 patients (21 %), including 3 patients (13 %) with cutaneous mastocytosis (CM), and 9 (28 %) with indolent systemic mastocytosis (ISM). IVA was confirmed in 13 patients (22.8 %) including 6 patients (10.5 %) with CM, and 7 patients (12.3 %) with ISM. Drug hypersensitivity was diagnosed in 10 patients (17.5 %). Significant differences in the gene expression were found for TRAF4 (p = 0.008) in the comparison of the mastocytosis patients with and without concomitant food hypersensitivity. Furthermore significant differences were found in gene expression for B3GAT1 (p = 0.003) in patients with IVA compared to patients without insect sting anaphylaxis in the medical history. The expression of studied genes did not differ according to the presence of drug hypersensitivity. The TRAF4 expression was higher in mastocytosis patients with food hypersensitivity in their medical history, the B3GAT1 expression was lower in mastocytosis patients with IVA in history.
[Mh] Termos MeSH primário: Hipersensibilidade Alimentar
Glucuronosiltransferase/metabolismo
Mordeduras e Picadas de Insetos/imunologia
Mastocitose Sistêmica/imunologia
Mastocitose/imunologia
Fator 4 Associado a Receptor de TNF/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Alérgenos
Anafilaxia/imunologia
Hipersensibilidade a Drogas
Feminino
Regulação da Expressão Gênica
Seres Humanos
Masculino
Mastocitose/metabolismo
Mastocitose Sistêmica/metabolismo
Meia-Idade
Peçonhas
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (TNF Receptor-Associated Factor 4); 0 (TRAF4 protein, human); 0 (Venoms); EC 2.4.1.135 (galactosylgalactoylxylosylprotein 3-beta-glucuronosyltransferase); EC 2.4.1.17 (Glucuronosyltransferase)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160418
[St] Status:MEDLINE


  4 / 90 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
[PMID]:26617938
[Au] Autor:Yang J; Wei D; Wang W; Shen B; Xu S; Cao Y
[Ad] Endereço:Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Xinxiang Medial University Weihui 453100, China.
[Ti] Título:TRAF4 enhances oral squamous cell carcinoma cell growth, invasion and migration by Wnt-ß-catenin signaling pathway.
[So] Source:Int J Clin Exp Pathol;8(9):11837-46, 2015.
[Is] ISSN:1936-2625
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oral squamous cell carcinoma (OSCC) ranks as the fifth most common cancer worldwide with poor prognosis. Recently, tumor necrosis factor receptor-associated factor 4 (TRAF4) has attracted increasing attenuation due to its overexpression in certain cancers. However, its function and underlying mechanism in OSCC remains elusive. In this study, the high expression of TRAF4 mRNA and protein levels was noted in OSCC cell lines. Its overexpression with pcDNA3.1-TRAF4 vector transfection dramatically promoted cell proliferation and inhibited cell apoptosis, indicating a pivotal role of TRAF4 in OSCC cell growth. Simultaneously, TRAF4 elevation also increased cell invasion and migration. Mechanism analysis confirmed that TRAF4 up-regulation induced the expression of ß-catenin and the downstream target molecules of cyclinD1, c-myc, Bcl-2, MMP-9 and MMP-2, indicating that TRAF4 could induce the activation of Wnt/ß-catenin pathway. After pretreatment with ß-catenin siRNA, the pathway was remarkably silenced. Simultaneously, cell growth, invasion and migration induced by TRAF4 were strikingly abrogated, suggesting that TRAF4 may promote OSCC cell growth, invasion and migration by Wnt/ß-catenin pathway. Together, this study confirmed that TRAF4 acts as an oncogene for the development and progression of OSCC. Therefore, our study may support a promising therapeutic target for the treatment of OSCC.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/metabolismo
Movimento Celular
Proliferação Celular
Neoplasias de Cabeça e Pescoço/metabolismo
Fator 4 Associado a Receptor de TNF/metabolismo
Neoplasias da Língua/metabolismo
Via de Sinalização Wnt
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Apoptose
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/patologia
Linhagem Celular Tumoral
Ciclina D1/metabolismo
Neoplasias de Cabeça e Pescoço/genética
Neoplasias de Cabeça e Pescoço/patologia
Seres Humanos
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Invasividade Neoplásica
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Proteínas Proto-Oncogênicas c-myc/metabolismo
Interferência de RNA
Fator 4 Associado a Receptor de TNF/genética
Neoplasias da Língua/genética
Neoplasias da Língua/patologia
Transfecção
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCL2 protein, human); 0 (CCND1 protein, human); 0 (CTNNB1 protein, human); 0 (MYC protein, human); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Proto-Oncogene Proteins c-myc); 0 (TNF Receptor-Associated Factor 4); 0 (TRAF4 protein, human); 0 (beta Catenin); 136601-57-5 (Cyclin D1); EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151201
[St] Status:MEDLINE


  5 / 90 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26383831
[Au] Autor:Jeanes A; Coulthard LG; Mantovani S; Markham K; Woodruff TM
[Ad] Endereço:School of Biomedical Sciences, University of Queensland, Australia.
[Ti] Título:Co-ordinated expression of innate immune molecules during mouse neurulation.
[So] Source:Mol Immunol;68(2 Pt A):253-60, 2015 Dec.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The innate immune system is the first line of defence against pathogens and infection. Recently, it has become apparent that many innate immune factors have roles outside of immunity and there is growing evidence that these factors play important functional roles during the development of a range of model organisms. Several studies have documented developmental expression of individual factors of the toll-like receptor and complement systems, and we recently demonstrated a key role for complement C5a receptor (C5aR1) signalling in neural tube closure in mice. Despite these emerging studies, a comprehensive expression analysis of these molecules in embryonic development is lacking. In the current study, we therefore, examined the expression of key innate immune factors in the early development period of neurulation (7.5-10.5dpc) in mice. We found that complement factor genes were differentially expressed during this period of murine development. Interestingly, the expression patterns we identified preclude activation of the classical and alternative pathways and formation of the membrane attack complex. Additionally, several other classes of innate immune molecules were expressed during the period of neurulation, including toll-like receptors (TLR-2, -3, -4 and -9), receptor for advanced glycation end-products (RAGE), and their signalling adapters (TRAF-4, TRAF-6, TAK-1 and MyD88). Taken together, this study highlights a number of innate immune factors as potential novel players in early embryonic development.
[Mh] Termos MeSH primário: Via Alternativa do Complemento/genética
Via Clássica do Complemento/genética
Lectina de Ligação a Manose da Via do Complemento/genética
Proteínas do Sistema Complemento/genética
Imunidade Inata
Neurulação/imunologia
[Mh] Termos MeSH secundário: Animais
Proteínas do Sistema Complemento/imunologia
Embrião de Mamíferos
Regulação da Expressão Gênica no Desenvolvimento
Hibridização In Situ
MAP Quinase Quinase Quinases/genética
MAP Quinase Quinase Quinases/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Fator 88 de Diferenciação Mieloide/genética
Fator 88 de Diferenciação Mieloide/imunologia
Neurulação/genética
Isoformas de Proteínas/genética
Isoformas de Proteínas/imunologia
Receptor para Produtos Finais de Glicação Avançada/genética
Receptor para Produtos Finais de Glicação Avançada/imunologia
Transdução de Sinais
Fator 4 Associado a Receptor de TNF/genética
Fator 4 Associado a Receptor de TNF/imunologia
Receptores Toll-Like/genética
Receptores Toll-Like/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ager protein, mouse); 0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); 0 (Protein Isoforms); 0 (Receptor for Advanced Glycation End Products); 0 (TNF Receptor-Associated Factor 4); 0 (Toll-Like Receptors); 9007-36-7 (Complement System Proteins); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 2.7.11.25 (MAP kinase kinase kinase 7)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150919
[St] Status:MEDLINE


  6 / 90 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26347473
[Au] Autor:Wu L; Chen X; Zhao J; Martin B; Zepp JA; Ko JS; Gu C; Cai G; Ouyang W; Sen G; Stark GR; Su B; Vines CM; Tournier C; Hamilton TA; Vidimos A; Gastman B; Liu C; Li X
[Ad] Endereço:Department of Immunology, Department of Anatomical Pathology and Clinical Pathology, Department of Cancer Biology, Department of Dermatology, and Department of Plastic Surgery, Cleveland Clinic, Cleveland, OH 44195 Department of Pathology and Department of Molecular Medicine, Cleveland Clinic Lerner
[Ti] Título:A novel IL-17 signaling pathway controlling keratinocyte proliferation and tumorigenesis via the TRAF4-ERK5 axis.
[So] Source:J Exp Med;212(10):1571-87, 2015 Sep 21.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although IL-17 is emerging as an important cytokine in cancer promotion and progression, the underlining molecular mechanism remains unclear. Previous studies suggest that IL-17 (IL-17A) sustains a chronic inflammatory microenvironment that favors tumor formation. Here we report a novel IL-17-mediated cascade via the IL-17R-Act1-TRAF4-MEKK3-ERK5 positive circuit that directly stimulates keratinocyte proliferation and tumor formation. Although this axis dictates the expression of target genes Steap4 (a metalloreductase for cell metabolism and proliferation) and p63 (a transcription factor for epidermal stem cell proliferation), Steap4 is required for the IL-17-induced sustained expansion of p63(+) basal cells in the epidermis. P63 (a positive transcription factor for the Traf4 promoter) induces TRAF4 expression in keratinocytes. Thus, IL-17-induced Steap4-p63 expression forms a positive feedback loop through p63-mediated TRAF4 expression, driving IL-17-dependent sustained activation of the TRAF4-ERK5 axis for keratinocyte proliferation and tumor formation.
[Mh] Termos MeSH primário: Interleucina-17/metabolismo
Queratinócitos/metabolismo
Queratinócitos/patologia
Proteína Quinase 7 Ativada por Mitógeno/metabolismo
Fator 4 Associado a Receptor de TNF/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/patologia
Proliferação Celular/genética
Retroalimentação Fisiológica
Seres Humanos
Interleucina-17/genética
MAP Quinase Quinase Quinase 3/genética
MAP Quinase Quinase Quinase 3/metabolismo
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Proteína Quinase 7 Ativada por Mitógeno/genética
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Receptores de Interleucina-17/genética
Receptores de Interleucina-17/metabolismo
Transdução de Sinais
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/patologia
Fator 4 Associado a Receptor de TNF/genética
Transativadores/genética
Transativadores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Interleukin-17); 0 (Membrane Proteins); 0 (Phosphoproteins); 0 (Receptors, Interleukin-17); 0 (TNF Receptor-Associated Factor 4); 0 (Tiarp protein, mouse); 0 (Traf3ip2 protein, mouse); 0 (Traf4 protein, mouse); 0 (Trans-Activators); 0 (Trp63 protein, mouse); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 7); EC 2.7.11.25 (MAP Kinase Kinase Kinase 3); EC 2.7.11.25 (Map3k3 protein, mouse)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150909
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20150204


  7 / 90 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26331901
[Au] Autor:Zhao ZJ; Ren HY; Yang F; Wang J; Wu GP; Mi XY
[Ad] Endereço:Department of Pathology, the First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning, China.
[Ti] Título:Expression, correlation, and prognostic value of TRAF2 and TRAF4 expression in malignant plural effusion cells in human breast cancer.
[So] Source:Diagn Cytopathol;43(11):897-903, 2015 Nov.
[Is] ISSN:1097-0339
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: TRAF2 and TRAF4, members of the tumor necrosis factor receptor- associated factor family of intracellular signal transduction proteins, are associated with breast cancer progression and metastasis. METHODS: We collected malignant serous effusion cells from the patients with breast cancer (n = 46). Cell blocks prepared from plural effusions (n = 46) and primary breast cancer (n = 50), lymph node metastases (n = 50), and normal breast tissue specimens (n = 30). The immunohistochemistry was performed for the detection of TRAF2 and TRAF4 expression with the correlation of their expression with clinicopathological parameters and survival rate analyzed. RESULTS: Compared with normal breast tissues, TRAF2 expression was upregulated, and nuclear TRAF4 expression was downregulated in malignant pleural effusion cells, primary tumors, and lymph node metastases (P < 0.05). Multivariate analysis revealed TRAF2 expression in pleural effusions was associated with the molecular/pathological type, venous invasion, and lymph node metastasis, while nuclear TRAF4 expression was associated with age, tumor size, venous invasion, and lymph node metastasis, clinical staging, molecular/pathological subtype and p53 status (P < 0.05). There was a significant positive correlation between TRAF2 and TRAF4 expression levels in malignant pleural effusion cells (r = 0.937; P < 0.01). Kaplan-Meire analysis demonstrated a close correlation of TRAF2 and TRAF4 expression in malignant pleural effusion cells with cumulative overall survival (P < 0.05). CONCLUSION: TRAF2 and nuclear TRAF4 expression in malignant pleural effusion cells may represent potential prognostic factors and biomarkers of invasion and metastasis in breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Regulação Neoplásica da Expressão Gênica/genética
Derrame Pleural Maligno/metabolismo
Fator 2 Associado a Receptor de TNF/metabolismo
Fator 4 Associado a Receptor de TNF/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Neoplasias da Mama/mortalidade
Feminino
Seres Humanos
Imuno-Histoquímica/métodos
Metástase Linfática
Meia-Idade
Derrame Pleural Maligno/etiologia
Derrame Pleural Maligno/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (TNF Receptor-Associated Factor 2); 0 (TNF Receptor-Associated Factor 4)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151014
[Lr] Data última revisão:
151014
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150903
[St] Status:MEDLINE
[do] DOI:10.1002/dc.23330


  8 / 90 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25976502
[Au] Autor:Chen T; Gao F; Feng S; Yang T; Chen M
[Ad] Endereço:Respiratory Department, The First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.
[Ti] Título:MicroRNA-370 inhibits the progression of non-small cell lung cancer by downregulating oncogene TRAF4.
[So] Source:Oncol Rep;34(1):461-8, 2015 Jul.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Lung cancer is the leading cause of cancer-related deaths, of which most can be attributed to non-small cell lung cancer (NSCLC). microRNAs (miRNAs) are a group of small non-coding RNAs that focus on post-transcriptional modification. The present study aimed to investigate the role and function of microRNA-370 (miR-370) in NSCLC and explore the underlying functional mechanisms. We found that miR-370 was significantly downregulated in the tumor tissues of NSCLC patients as well as in NSCLC cell lines. Overexpression of miR-370 by infection of recombinant lentivirus markedly inhibited cell proliferation and promoted cell apoptosis of NSCLC cells. In addition, in vivo tumor formation of NSCLC cells was decreased by miR-370 overexpression. Through bioinformatic analysis, we found that tumor necrosis factor receptor-associated factor 4 (TRAF4), an oncogene as previously reported, was predicted as a putative target gene of miR-370. The direct targeting relationship between miR-370 and the 3'-untranslated region was validated by dual-luciferase reporter assay. Furthermore, overexpression of miR-370 downregulated the protein expression of TRAF4 in the NSCLC cells. Moreover, the growth inhibitory effect of miR-370 overexpression on NSCLC cells was abrogated by TRAF4 overexpression. In conclusion, our results suggest that miR-370 plays an important role in NSCLC by regulating TRAF4 and may be a potential target for the treatment of NSCLC.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/patologia
Neoplasias Pulmonares/patologia
MicroRNAs/genética
MicroRNAs/metabolismo
Fator 4 Associado a Receptor de TNF/genética
Fator 4 Associado a Receptor de TNF/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Proteínas Reguladoras de Apoptose
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Progressão da Doença
Regulação para Baixo
Feminino
Seres Humanos
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Proteínas Mitocondriais
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Apop-1 protein, mouse); 0 (Apoptosis Regulatory Proteins); 0 (MIRN370 microRNA, human); 0 (MicroRNAs); 0 (Mitochondrial Proteins); 0 (TNF Receptor-Associated Factor 4); 0 (TRAF4 protein, human)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150611
[Lr] Data última revisão:
150611
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150516
[St] Status:MEDLINE
[do] DOI:10.3892/or.2015.3978


  9 / 90 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
[PMID]:25973026
[Au] Autor:Yang K; Wang F; Han JJ
[Ad] Endereço:Department of Liver General Surgery, Nan Yang Central Hospital Nan Yang 473003, Henan Province, China.
[Ti] Título:TRAF4 promotes the growth and invasion of colon cancer through the Wnt/ß-catenin pathway.
[So] Source:Int J Clin Exp Pathol;8(2):1419-26, 2015.
[Is] ISSN:1936-2625
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor necrosis factor receptor-associated factor 4 (TRAF4) has been linked to carcinogenesis. However, the role of TRAF4 in colon cancer is still unclear. Therefore, we investigated the role of TRAF4 in colon cancer and the underlying mechanism. In the present study, we found that TRAF4 was overexpressed in colon cancer tissues and cells, and small interfering RNA (siRNA)-mediated gene knockdown of TRAF4 significantly inhibited cell proliferation, invasion and tumorigenesis, both in vitro and in vivo, but induced apoptosis in colon cancer cells. Furthermore, siRNA-TRAF4 significantly inhibited the expression levels of ß-catenin, cyclinD1, and c-myc proteins in colon cancer cells. Taken together, these results suggest that TRAF4 promoted colon cancer cell growth and invasion by potentiating the Wnt/ß-catenin pathway, suggesting that TRAF4 may be a potential molecular target for colon cancer prevention and therapy.
[Mh] Termos MeSH primário: Proliferação Celular
Neoplasias do Colo/patologia
Fator 4 Associado a Receptor de TNF/biossíntese
Via de Sinalização Wnt/fisiologia
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Western Blotting
Linhagem Celular Tumoral
Técnicas de Silenciamento de Genes
Xenoenxertos
Seres Humanos
Camundongos
Camundongos Nus
Invasividade Neoplásica
RNA Interferente Pequeno
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (TNF Receptor-Associated Factor 4); 0 (TRAF4 protein, human)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150515
[St] Status:MEDLINE


  10 / 90 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
[PMID]:25738361
[Au] Autor:Ren HY; Wang J; Yang F; Zhang XL; Wang AL; Sun LL; Diao KX; Wang EH; Mi XY
[Ad] Endereço:Department of Pathology, First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang 110001, P.R. China.
[Ti] Título:Cytoplasmic TRAF4 contributes to the activation of p70s6k signaling pathway in breast cancer.
[So] Source:Oncotarget;6(6):4080-96, 2015 Feb 28.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor receptor associated factor 4 (TRAF4) is an important adaptor protein that plays a significant role in several signaling pathways. By studying the relationship between TRAF4 and 70 kDa ribosomal protein S6 kinase (p70s6k) in vivo, we demonstrated that cytoplasmic TRAF4 was correlated with the activation of p70s6k in breast cancer. Moreover, we found that cytoplasmic TRAF4 expression in breast cancer patients was significantly associated with a poor prognosis. To determine the exact mechanism, we analyzed the interaction between TRAF4 and p70s6k and identified the Zinc fingers domain of TRAF4 was responsible for their interaction in MCF7 cells. Furthermore, we found that activation of p70s6k/S6 signaling pathway by TRAF4 requires the mammalian target of rapamycin (mTOR) activity; TRAF4 acted as a sensitizer. Tumor necrosis factor receptor associated factor 2 (TRAF2), as a binding partner of TRAF4, could also promoted activation of p70s6k signaling via upregulating cytoplasm expression of TRAF4 and played a critical role in TNFa-induced activation of p70s6k/S6 pathway. Finally, we demonstrated p70s6k/S6 signaling pathway played an important role in the promoting function of TRAF4 on cell proliferation. In summary, our work suggests a new direction for understanding the oncogenic function of TRAF4 in breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Proteínas Quinases S6 Ribossômicas 70-kDa/metabolismo
Fator 4 Associado a Receptor de TNF/metabolismo
[Mh] Termos MeSH secundário: Neoplasias da Mama/patologia
Proliferação Celular/fisiologia
Citoplasma/metabolismo
Feminino
Seres Humanos
Células MCF-7
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (TNF Receptor-Associated Factor 4); 0 (TRAF4 protein, human); EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:150509
[Lr] Data última revisão:
150509
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150305
[St] Status:MEDLINE



página 1 de 9 ir para página                      
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde