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Pesquisa : D12.776.543.750.725.937 [Categoria DeCS]
Referências encontradas : 327 [refinar]
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[PMID]:28143891
[Au] Autor:Lu TP; Chuang NC; Cheng CY; Hsu CA; Wang YC; Lin YH; Lee JK; Wu CK; Hwang JJ; Lin LY; Yeh SS; Chien KL; Juang JJ
[Ad] Endereço:Institute of Epidemiology and Preventive Medicine, Department of Public Health, National Taiwan University, Taiwan.
[Ti] Título:Genome-wide methylation profiles in coronary artery ectasia.
[So] Source:Clin Sci (Lond);131(7):583-594, 2017 Apr 01.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Coronary artery ectasia (CAE) is a disease characterized by abnormally dilated coronary arteries. The mechanism of CAE remains unclear, and its treatment is limited. Previous studies have shown that risk factors for CAE were related to changes in DNA methylation. However, no systematic investigation of methylation profiles has been performed. Therefore, we compared methylation profiles between 12 CAE patients and 12 propensity-matched individuals with normal coronary arteries using microarrays. Wilcoxon's rank sum tests revealed 89 genes with significantly different methylation levels ( <0.05 and Δß > |0.1|). Functional characterization using the DAVID database and gene set enrichment analysis indicated that these genes were involved in immune and inflammatory responses. Of these genes 6 were validated in 29 CAE patients and 87 matched individuals with CAE, using pyro-sequencing. and showed significant differences in methylation between the two groups, and lower protein levels of toll-like receptor 6 (TLR6) were detected in CAE patients. In conclusion, this genome-wide analysis of methylation profiles in CAE patients showed that significant changes in both methylation and expression of deserve further study to elucidate their roles in CAE.
[Mh] Termos MeSH primário: Doença da Artéria Coronariana/genética
Vasos Coronários/patologia
Metilação de DNA
[Mh] Termos MeSH secundário: Adulto
Idoso
Estudos de Casos e Controles
Doença da Artéria Coronariana/imunologia
Dilatação Patológica/genética
Dilatação Patológica/imunologia
Feminino
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla/métodos
Seres Humanos
Inflamação/genética
Masculino
Meia-Idade
Proteínas Proto-Oncogênicas/genética
Receptor Notch4
Receptores Notch/genética
Receptor 6 Toll-Like/sangue
Receptor 6 Toll-Like/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NOTCH4 protein, human); 0 (Proto-Oncogene Proteins); 0 (Receptor, Notch4); 0 (Receptors, Notch); 0 (TLR6 protein, human); 0 (Toll-Like Receptor 6)
[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:170202
[St] Status:MEDLINE
[do] DOI:10.1042/CS20160821


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[PMID]:28108315
[Au] Autor:Bui QT; Im JH; Jeong SB; Kim YM; Lim SC; Kim B; Kang KW
[Ad] Endereço:College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea.
[Ti] Título:Essential role of Notch4/STAT3 signaling in epithelial-mesenchymal transition of tamoxifen-resistant human breast cancer.
[So] Source:Cancer Lett;390:115-125, 2017 Apr 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:We previously demonstrated that tamoxifen (TAM)-resistant human breast cancer (TAMR-MCF-7) cells showed increased expression of mesenchymal marker proteins compared to the parent MCF-7 cells. Notch is functionally important in the promotion of epithelial-mesenchymal transition (EMT) during both development and tumor progression. Notch1 and Notch4 have been reported as prognostic markers in human breast cancer. Here, we indicated that Notch4, but not Notch1, plays a critical role in the regulation of EMT signaling in TAMR-MCF-7 cells. Notch4 suppression by either Notch inhibitors or Notch4 siRNA attenuated EMT signaling. Tyrosine-phosphorylated STAT3 protein is known as a crucial signaling molecule in the regulation of tumorigenesis and metastasis. We found that TAMR-MCF-7 cells exhibited constitutive STAT3 phosphorylation, and Notch inhibition reduced the level of activated STAT3 in TAMR-MCF-7 cells. An intrasplenic injection model of liver metastases was performed using TAMR-MCF-7 cells. Mice injected with N-[N-(3,5-Difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester (DAPT, 10 mg/kg) formed smaller splenic tumors and showed a reduced micrometastatic tumor burden in their livers compared with the control group treated with vehicle. To conclude, Notch4 could be a potential target to prevent metastasis in TAM-resistant breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/fisiopatologia
Transição Epitelial-Mesenquimal/fisiologia
Proteínas Proto-Oncogênicas/metabolismo
Receptores Notch/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais/fisiologia
Tamoxifeno/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Hormonais/farmacologia
Antineoplásicos Hormonais/uso terapêutico
Neoplasias da Mama/tratamento farmacológico
Linhagem Celular Tumoral
Proliferação Celular
Resistência a Medicamentos Antineoplásicos/genética
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Feminino
Seres Humanos
Immunoblotting
Camundongos Nus
Reação em Cadeia da Polimerase
Ligação Proteica
Proteínas Proto-Oncogênicas/antagonistas & inibidores
Receptor Notch4
Receptores Notch/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Tamoxifeno/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (NOTCH4 protein, human); 0 (Proto-Oncogene Proteins); 0 (Receptor, Notch4); 0 (Receptors, Notch); 0 (STAT3 Transcription Factor); 094ZI81Y45 (Tamoxifen)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170122
[St] Status:MEDLINE


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[PMID]:28061457
[Au] Autor:Xiong J; Zhang X; Chen X; Wei Y; Lu DG; Han YW; Xu J; Yu D
[Ad] Endereço:Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province 330006, P. R. China.
[Ti] Título:Prognostic roles of mRNA expression of notch receptors in non-small cell lung cancer.
[So] Source:Oncotarget;8(8):13157-13165, 2017 Feb 21.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Notch signalling is aberrantly activated in human non-small cell lung cancer (NSCLC). Nevertheless, the prognostic roles of mRNA expression of four Notch receptors in NSCLC patients remain elusive. In this report, we reported the prognostic roles of Notch receptors in a total of 1,926 NSCLC patients through "The Kaplan-Meier plotter" (KM plotter) database which is capable to assess the effect of 22,277 genes on survival of NSCLC patients. We found that mRNA high expression level of Notch1 was associated with better overall survival (OS) for all NSCLC patients, hazard ratio (HR) 0.78 (0.69-0.89), p=0.00019, better OS in adenocarcinoma (Ade) patients, HR 0.59 (0.46-0.75), p=1.5e-05, as well as in squamous cell carcinoma (SCC) patients, HR 0.78 (0.62-0.99), p=0.044. mRNA high expression levels of Notch2 and Notch3 were associated with worsen OS for all NSCLC patients, as well as in Ade, but not in SCC patients. mRNA high expression level of Notch4 was not found to be associated with to OS for all NSCLC patients. In addition, mRNA high expression levels of Notch2, Notch3, but Notch4 are significantly associated with the NSCLC patients who have different smoking status. Our results indicate that mRNA expression of Notch receptors may have distinct prognostic values in NSCLC patients. These results will benefit for developing tools to accurately predict the prognosis of NSCLC patients.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/genética
Regulação Neoplásica da Expressão Gênica
Neoplasias Pulmonares/genética
RNA Mensageiro/genética
Receptores Notch/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/tratamento farmacológico
Adenocarcinoma/genética
Adenocarcinoma/patologia
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Carcinoma Pulmonar de Células não Pequenas/patologia
Carcinoma de Células Escamosas/tratamento farmacológico
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/patologia
Perfilação da Expressão Gênica/métodos
Seres Humanos
Estimativa de Kaplan-Meier
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/patologia
Avaliação de Resultados (Cuidados de Saúde)/métodos
Avaliação de Resultados (Cuidados de Saúde)/estatística & dados numéricos
Prognóstico
Modelos de Riscos Proporcionais
Proteínas Proto-Oncogênicas/genética
Receptor Notch1/genética
Receptor Notch2/genética
Receptor Notch3/genética
Receptor Notch4
Fumar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NOTCH1 protein, human); 0 (NOTCH2 protein, human); 0 (NOTCH3 protein, human); 0 (NOTCH4 protein, human); 0 (Proto-Oncogene Proteins); 0 (RNA, Messenger); 0 (Receptor, Notch1); 0 (Receptor, Notch2); 0 (Receptor, Notch3); 0 (Receptor, Notch4); 0 (Receptors, Notch)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.14483


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[PMID]:27840976
[Au] Autor:Yang SL; Ren QG; Zhang T; Pan X; Wen L; Hu JL; Yu C; He QJ
[Ad] Endereço:Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
[Ti] Título:Hepatitis B virus X protein and hypoxia­inducible factor-1α stimulate Notch gene expression in liver cancer cells.
[So] Source:Oncol Rep;37(1):348-356, 2017 Jan.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Increasing evidence has demonstrated that Notch genes, including Notch1, Notch2, Notch3 and Notch4, are involved in carcinogenesis. However, the expression and regulation of Notch genes in hepatocellular carcinoma (HCC) tissues have not been fully investigated. In the present study, immunohistochemical and quantitative real-time PCR (qPCR) analyses were performed to examine the expression of Notch genes in normal human liver, HBV-related HCC and paired peritumoral tissues. Additionally, qPCR and western blotting were utilized to investigate the impact of hepatitis B virus X protein (HBx) and hypoxia­inducible factor-1α (HIF-1α) on the regulation of Notch gene expression. The immunohistochemical and qPCR results showed that the expression levels of Notch1, Notch3 and Notch4 were significantly higher in HCC tissues than the levels in peritumoral and normal liver tissues. However, no significant difference in Notch2 expression was found between HCC and peritumoral tissues. Among the four Notch genes, immunohistochemical analyses found that only the increased level of Notch3 in HCC tissues was positively correlated with vascular invasion of liver cancer (P<0.05). Moreover, we found that overexpression of both HBx and HIF-1α increased the expression of Notch1, Notch3 and Notch4 in HepG2 and Bel-7404 cell lines. In summary, the present study demonstrated that Notch1, Notch3 and Notch4 were upregulated in HCC tissues and that HBx and HIF-1α may be the factors that cause the overexpression of Notch genes. Furthermore, the increased expression of Notch3 was closely related to the vascular invasiveness of HCC.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Neoplasias Hepáticas/genética
Receptores Notch/genética
Transativadores/metabolismo
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/virologia
Linhagem Celular Tumoral
Feminino
Regulação Neoplásica da Expressão Gênica
Vírus da Hepatite B/patogenicidade
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Neoplasias Hepáticas/virologia
Masculino
Meia-Idade
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas/metabolismo
Receptor Notch1/genética
Receptor Notch1/metabolismo
Receptor Notch2/genética
Receptor Notch2/metabolismo
Receptor Notch3/genética
Receptor Notch3/metabolismo
Receptor Notch4
Receptores Notch/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (NOTCH1 protein, human); 0 (NOTCH2 protein, human); 0 (NOTCH3 protein, human); 0 (NOTCH4 protein, human); 0 (Proto-Oncogene Proteins); 0 (Receptor, Notch1); 0 (Receptor, Notch2); 0 (Receptor, Notch3); 0 (Receptor, Notch4); 0 (Receptors, Notch); 0 (Trans-Activators); 0 (hepatitis B virus X protein)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161115
[St] Status:MEDLINE
[do] DOI:10.3892/or.2016.5211


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[PMID]:28013300
[Au] Autor:Wang H; Xia Y; Fu S; Wang W; Xie C; Zhang Y; Gong F
[Ad] Endereço:The Children's Hospital of Zhejiang University School of Medicine, Hangzhou, PR China.
[Ti] Título:Notch4 Signaling Pathway of Endothelial Progenitor Cells in a Kawasaki Disease Model Induced by Lactobacillus casei Cell Wall Extract.
[So] Source:J Vasc Res;53(5-6):340-348, 2016.
[Is] ISSN:1423-0135
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The Notch4 signaling pathway of endothelial progenitor cells (EPCs) may play a crucial role in Kawasaki disease (KD). We investigated the proliferation, adhesion, migration, angiogenesis, and expression levels of Notch4, recombination signal-binding protein-Jκ (RBP-Jκ), P-selectin, and vascular cell adhesion molecule-1 (VCAM-1) of bone marrow (BM) EPCs in a KD model induced by Lactobacillus casei cell wall extract. The numbers of BM EPCs decreased significantly in the KD models. The Notch4 expression level on the EPC surface was higher in the KD models than in the controls. The proliferative, adhesive, migratory, and angiogenic properties, and double immunofluorescence-binding rate of BM EPCs were significantly impaired in the KD models. The levels of Notch4 and P-selectin mRNA were lower in the KD models than in the controls on day 3. The RBP-Jκ mRNA levels were lower in the KD models than in the controls on days 3 and 7. The levels of RBP-Jκ and vascular endothelial growth factor receptor-2 proteins decreased in the early stage. In conclusion, the BM EPC functions and bioactivities in the KD models were impaired, and the Notch4 signaling pathway is associated with KD.
[Mh] Termos MeSH primário: Parede Celular
Células Progenitoras Endoteliais/metabolismo
Lactobacillus casei
Síndrome de Linfonodos Mucocutâneos/metabolismo
Proteínas Proto-Oncogênicas/metabolismo
Receptores Notch/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Adesão Celular
Movimento Celular
Proliferação Celular
Células Cultivadas
Modelos Animais de Doenças
Células Progenitoras Endoteliais/patologia
Proteína de Ligação a Sequências Sinal de Recombinação J de Imunoglobina/metabolismo
Masculino
Camundongos Endogâmicos BALB C
Síndrome de Linfonodos Mucocutâneos/induzido quimicamente
Síndrome de Linfonodos Mucocutâneos/genética
Síndrome de Linfonodos Mucocutâneos/patologia
Selectina-P/metabolismo
Fenótipo
Proteínas Proto-Oncogênicas/genética
Receptor Notch4
Receptores Notch/genética
Fatores de Tempo
Molécula 1 de Adesão de Célula Vascular/metabolismo
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin J Recombination Signal Sequence-Binding Protein); 0 (P-Selectin); 0 (Proto-Oncogene Proteins); 0 (Rbpj protein, mouse); 0 (Receptor, Notch4); 0 (Receptors, Notch); 0 (Vascular Cell Adhesion Molecule-1); 146991-60-8 (Notch4 protein, mouse); EC 2.7.10.1 (Kdr protein, mouse); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161226
[St] Status:MEDLINE
[do] DOI:10.1159/000449061


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[PMID]:27906177
[Au] Autor:Abu-Tayeh H; Weidenfeld K; Zhilin-Roth A; Schif-Zuck S; Thaler S; Cotarelo C; Tan TZ; Thiery JP; Green JE; Klorin G; Sabo E; Sleeman JP; Tzukerman M; Barkan D
[Ad] Endereço:Department of Human Biology, University of Haifa, Haifa, Israel.
[Ti] Título:'Normalizing' the malignant phenotype of luminal breast cancer cells via alpha(v)beta(3)-integrin.
[So] Source:Cell Death Dis;7(12):e2491, 2016 Dec 01.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Reestablishing tissue organization of breast cancer cells into acini was previously shown to override their malignant phenotype. In our study, we demonstrate that alpha(v)beta(3) integrin (Int-αvß3), previously shown to play a role in cancer progression, promoted differentiation and growth arrest of organoids derived from luminal A breast cancer cells grown in their relevant three-dimensional microenvironment. These organoids differentiated into normal-like acini resembling a benign stage of breast tissue. Likewise, we demonstrate that Int-αvß3 is selectively expressed in the epithelium of the benign stage of breast tissues, and is lost during the early stages of luminal A breast cancer progression. Notably, the organoids' reversion into normal-like acini was mediated by cancer luminal progenitor-like cells expressing both EpCAM CD49f CD24 and Int-αvß3. Furthermore, downregulation of Notch4 expression and downstream signaling was shown to mediate Int-αvß3-induced reversion. Intriguingly, when luminal A breast cancer cells expressing Int-αvß3 were injected into a humanized mouse model, differentiated tumors developed when compared with that generated by control cells. Hence, our data suggest that promoting differentiation of luminal A breast cancer cells by signaling emanating from Int-αvß3 can potentially promote 'normalization' of their malignant phenotype and may prevent the malignant cells from progressing.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Integrina alfaVbeta3/metabolismo
[Mh] Termos MeSH secundário: Células Acinares/metabolismo
Células Acinares/patologia
Membrana Basal/metabolismo
Diferenciação Celular
Linhagem Celular Tumoral
Proliferação Celular
Regulação para Baixo
Células-Tronco Embrionárias/metabolismo
Feminino
Técnicas de Silenciamento de Genes
Seres Humanos
Hiperplasia
Células MCF-7
Células-Tronco Neoplásicas/metabolismo
Células-Tronco Neoplásicas/patologia
Organoides/metabolismo
Organoides/patologia
Fenótipo
Proteínas Proto-Oncogênicas/metabolismo
Receptor Notch4
Receptores Notch/metabolismo
Transdução de Sinais
Esferoides Celulares/metabolismo
Esferoides Celulares/patologia
Teratoma/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alphaVbeta3); 0 (NOTCH4 protein, human); 0 (Proto-Oncogene Proteins); 0 (Receptor, Notch4); 0 (Receptors, Notch)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161202
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2016.387


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[PMID]:27431799
[Au] Autor:Cheung CC; Lun SW; Chung GT; Chow C; Lo C; Choy KW; Lo KW
[Ad] Endereço:Department of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong.
[Ti] Título:MicroRNA-183 suppresses cancer stem-like cell properties in EBV-associated nasopharyngeal carcinoma.
[So] Source:BMC Cancer;16:495, 2016 07 19.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Nasopharyngeal carcinoma (NPC) is an Epstein-Barr virus (EBV)-associated epithelial malignancy that exhibits distinct geographical and ethnic prevalence. Although the contemporary therapeutic approach of radio-/chemotherapy provides excellent results for patients with early-stage disease, it is far from satisfactory for those with disease remission and distant metastasis. Promising therapeutic strategies for advanced and relapsed NPC are still lacking. We recently identified and characterized a cancer stem-like cell (CSC) subpopulation in NPC that appeared to play an important role in tumor progression. Microarray analysis revealed downregulation of several stemness-inhibiting miRNAs in these CSC cells. Among these miRNAs, miR-96 and miR-183 showed the highest fold change and were selected to elucidate their role in repressing NPC CSC properties. METHODS: MiR-96 and miR-183 expression in NPC CSCs was detected by qRT-PCR. Transient and stable transfection was performed in EBV-positive NPC C666-1 cells to examine the effects of ectopic expression of miR-96 and miR-183 on repressing cell growth and CSC properties. Anchorage-dependent (colony formation) and anchorage-independent (tumor sphere formation) growths of these miR-96 and miR-183 expressing cells were determined. Expression of multiple CSC markers and related molecules were accessed by flow cytometry and Western blotting. The tumorigenicity of the stable miR-96- and miR-183-transfected NPC cells was examined in an in vivo nude mice model. RESULTS: Downregulation of miR-96 and miR-183 was confirmed in NPC spheroids. Using transient or stable transfection, we showed that ectopic expression of miR-96 and miR-183 suppressed cell growth and tumor sphere formation in NPC. Reduced NICD3 and NICD4 in miR-96- and miR-183-expressing NPC cells suggests the involvement of the NOTCH signaling pathway in their tumor suppressive function. Finally, we showed that the tumorigenicity of cells stably expressing miR-183 was significantly inhibited in the in vivo nude mice model. CONCLUSIONS: miR-183 is a tumor-suppressive miRNA in EBV-associated NPC. Its abilities to suppress CSC properties in vitro and effectively reduce tumor growth in vivo shed light on its role as a potential therapeutic target.
[Mh] Termos MeSH primário: Infecções por Vírus Epstein-Barr/genética
Regulação Neoplásica da Expressão Gênica
MicroRNAs/genética
Neoplasias Nasofaríngeas/genética
Células-Tronco Neoplásicas/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular Tumoral
Ciclina D1/genética
Ciclina D1/metabolismo
Infecções por Vírus Epstein-Barr/metabolismo
Infecções por Vírus Epstein-Barr/virologia
Feminino
Herpesvirus Humano 4/fisiologia
Interações Hospedeiro-Patógeno
Seres Humanos
Camundongos Endogâmicos BALB C
Camundongos Nus
Neoplasias Nasofaríngeas/metabolismo
Neoplasias Nasofaríngeas/virologia
Células-Tronco Neoplásicas/virologia
Análise de Sequência com Séries de Oligonucleotídeos
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas/metabolismo
Receptor Notch3/genética
Receptor Notch3/metabolismo
Receptor Notch4
Receptores Notch/genética
Receptores Notch/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Esferoides Celulares/metabolismo
Esferoides Celulares/virologia
Transplante Heterólogo/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCND1 protein, human); 0 (MIRN183 microRNA, human); 0 (MIRN96 microRNA, human); 0 (MicroRNAs); 0 (NOTCH3 protein, human); 0 (NOTCH4 protein, human); 0 (Proto-Oncogene Proteins); 0 (Receptor, Notch3); 0 (Receptor, Notch4); 0 (Receptors, Notch); 136601-57-5 (Cyclin D1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160720
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-016-2525-5


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[PMID]:27354212
[Au] Autor:Alabi RO; Glomski K; Haxaire C; Weskamp G; Monette S; Blobel CP
[Ad] Endereço:From the Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY (R.O.A., K.G., C.H., G.W., C.P.B.); Weill Cornell/Rockefeller/Sloan-Kettering Tri-Institutional MD-PhD Program, New York, NY (R.O.A., K.G., C.P.B.); Tri-Institutional Laboratory of Comparative Pathology, M
[Ti] Título:ADAM10-Dependent Signaling Through Notch1 and Notch4 Controls Development of Organ-Specific Vascular Beds.
[So] Source:Circ Res;119(4):519-31, 2016 Aug 05.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Endothelial Notch signaling is critical for early vascular development and survival. Yet, previously described mice lacking endothelial a disintegrin and metalloproteinase 10 (ADAM10), a key regulator of Notch signaling, survived into adulthood with organ-specific vascular defects. These findings raised questions about whether these vascular defects were related to Notch signaling or other functions of ADAM10. OBJECTIVE: The aims of the study are to determine whether compensatory or redundant functions of ADAM17 in Notch signaling can explain the survival of Adam10ΔEC mice, explore the contribution of different Tie2-Cre transgenes to the differences in survival, and establish whether the Adam10ΔEC vascular phenotypes can be recapitulated by inactivation of Notch receptors in endothelial cells. METHODS AND RESULTS: Mice lacking ADAM10 and ADAM17 in endothelial cells (Adam10/Adam17ΔEC), which survived postnatally with organ-specific vascular defects, resembled Adam10ΔEC mice. In contrast, Adam10ΔEC mice generated with the Tie2Cre transgene previously used to inactivate endothelial Notch (Adam10ΔEC(Flv)) died by E10.5. Quantitative polymerase chain reaction analysis demonstrated that Cre-mediated recombination occurs earlier in Adam10ΔEC(Flv) mice than in the previously described Adam10ΔEC mice. Finally, mice lacking endothelial Notch1 (Notch1ΔEC) share some organ-specific vascular defects with Adam10ΔEC mice, whereas Notch4(-/-) mice lacking endothelial Notch1 (Notch1ΔEC/Notch4(-/-)) had defects in all vascular beds affected in Adam10ΔEC mice. CONCLUSIONS: Our results argue against a major role for ADAM17 in endothelial Notch signaling and clarify the difference in phenotypes of previously described mice lacking ADAM10 or Notch in endothelial cells. Most notably, these findings uncover new roles for Notch signaling in the development of organ-specific vascular beds.
[Mh] Termos MeSH primário: Proteína ADAM10/fisiologia
Secretases da Proteína Precursora do Amiloide/fisiologia
Circulação Sanguínea/fisiologia
Proteínas de Membrana/fisiologia
Proteínas Proto-Oncogênicas/fisiologia
Receptor Notch1/fisiologia
Receptores Notch/fisiologia
Fluxo Sanguíneo Regional/fisiologia
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Proteína ADAM10/deficiência
Secretases da Proteína Precursora do Amiloide/deficiência
Animais
Células Endoteliais/fisiologia
Feminino
Proteínas de Membrana/deficiência
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Gravidez
Proteínas Proto-Oncogênicas/deficiência
Receptor Notch1/deficiência
Receptor Notch4
Receptores Notch/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Notch1 protein, mouse); 0 (Proto-Oncogene Proteins); 0 (Receptor, Notch1); 0 (Receptor, Notch4); 0 (Receptors, Notch); 146991-60-8 (Notch4 protein, mouse); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (Adam10 protein, mouse)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160630
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.115.307738


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[PMID]:27234159
[Au] Autor:Lin X; Sun B; Zhu D; Zhao X; Sun R; Zhang Y; Zhang D; Dong X; Gu Q; Li Y; Liu F
[Ad] Endereço:Department of Pathology, Tianjin Medical University, Tianjin, China.
[Ti] Título:Notch4+ cancer stem-like cells promote the metastatic and invasive ability of melanoma.
[So] Source:Cancer Sci;107(8):1079-91, 2016 Aug.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Sphere formation in conditioned serum-free culture medium supplemented with epidermal growth factor and basic fibroblast growth factor (tumorospheres) is considered useful for the enrichment of cancer stem-like cells, also known as tumor-initiating cells. We used a gene expression microarray to investigate the gene expression profile of melanoma cancer stem-like cells (MCSLCs). The results showed that MCSLCs highly expressed the following Notch signaling pathway molecules: Notch3 (NM_008716), Notch4 (NM_010929), Dtx4 (NM_172442), and JAG2 (NM_010588). Immunofluorescence staining showed tumorosphere cells highly expressed Notch4. Notch4(high) B16F10 cells were isolated by FACS, and Western blotting showed that high Notch4 expression is related to the expression of epithelial-mesenchymal transition (EMT)-associated proteins. Reduced invasive and migratory properties concomitant with the downregulation of the EMT markers Twist1, vimentin, and VE-cadherin and the overexpression of E-cadherin was observed in human melanoma A375 and MUM-2B cells. In these cells, Notch4 was also downregulated, both by Notch4 gene knockdown and by application of the γ-secretase inhibitor, DAPT. Mechanistically, the re-overexpression of Twist1 by the transfection of cells with a Twist1 expression plasmid led to an increase in VE-cadherin expression and a decrease in E-cadherin expression. Immunohistochemical analysis of 120 human melanoma tissues revealed a significant correlation between the high expression of Notch4 and the metastasis of melanoma. Taken together, our findings indicate that Notch4+ MCSLCs trigger EMT and promote the metastasis of melanoma cells.
[Mh] Termos MeSH primário: Melanoma/metabolismo
Melanoma/patologia
Invasividade Neoplásica
Metástase Neoplásica
Células-Tronco Neoplásicas/metabolismo
Células-Tronco Neoplásicas/patologia
Proteínas Proto-Oncogênicas/metabolismo
Receptores Notch/metabolismo
[Mh] Termos MeSH secundário: Caderinas/metabolismo
Linhagem Celular Tumoral
Transição Epitelial-Mesenquimal/genética
Seres Humanos
Melanoma/genética
Invasividade Neoplásica/genética
Metástase Neoplásica/genética
Proteínas Nucleares/metabolismo
Proteínas Proto-Oncogênicas/deficiência
Proteínas Proto-Oncogênicas/genética
Receptor Notch4
Receptores Notch/deficiência
Receptores Notch/genética
Proteína 1 Relacionada a Twist/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (NOTCH4 protein, human); 0 (Nuclear Proteins); 0 (Proto-Oncogene Proteins); 0 (Receptor, Notch4); 0 (Receptors, Notch); 0 (TWIST1 protein, human); 0 (Twist-Related Protein 1)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160529
[St] Status:MEDLINE
[do] DOI:10.1111/cas.12978


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[PMID]:27197026
[Au] Autor:Mk H; Prince S; Mohan AM; Krishnan KV; Devi A
[Ad] Endereço:Department of Genetic Engineering, School of Bioengineering, SRM University, Kattankulathur 603203, India.
[Ti] Título:Association of Notch4 with metastasis in human oral squamous cell carcinoma.
[So] Source:Life Sci;156:38-46, 2016 Jul 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Despite the development of several therapeutic strategies in the past decades, clinicians have failed to improve the survival rate of oral squamous cell carcinoma patients due to the highly metastatic nature of the disease and its high recurrence rate. However, there is accumulating evidence that aberrant Notch4 expression has a critical role in tumorigenesis but its prognostic value and function in OSCC remains uncertain. This study therefore investigates (1) the expression of Notch4 and its downstream target, myelin associated glycoprotein (MAG) in tissue samples representative of different stages of OSCC with varied clinicopathological features and (2) the possible involvement of Notch4 in the proliferation and migration of OSCC cells. MAIN METHODS: Sixty patients reported positive for OSCC were obtained along with the clinicopathological parameters and we performed immunohistochemistry, western blotting and RT-PCR for Notch4 and MAG expression. Further, the metastatic role of Notch4 was analyzed in the HSC-3 cell line by cell proliferation and migration assays. KEY FINDINGS: Our findings reveal that Notch4 and MAG expression are significantly upregulated in specifically late stages of OSCC tumor sections and perineural invasion (PNI) positive cases. In addition, depletion of Notch4 by siRNA inhibited the proliferative and migratory ability of the highly metastatic HSC-3 OSCC cells. SIGNIFICANCE: Our study indicates that the aberrant activation of Notch4 promotes OSCC metastasis through perineural spread and ascertains its value as a significant prognostic marker and potential therapeutic target to treat this highly aggressive malignancy.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/patologia
Neoplasias Bucais/metabolismo
Neoplasias Bucais/patologia
Proteínas Proto-Oncogênicas/metabolismo
Receptores Notch/metabolismo
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/genética
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Meia-Idade
Neoplasias Bucais/genética
Glicoproteína Associada a Mielina/metabolismo
Invasividade Neoplásica
Metástase Neoplásica
Proteínas Proto-Oncogênicas/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptor Notch4
Receptores Notch/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MAG protein, human); 0 (Myelin-Associated Glycoprotein); 0 (NOTCH4 protein, human); 0 (Proto-Oncogene Proteins); 0 (RNA, Messenger); 0 (Receptor, Notch4); 0 (Receptors, Notch)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160520
[St] Status:MEDLINE



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