Base de dados : MEDLINE
Pesquisa : D12.776.543.750.705.408.100.400 [Categoria DeCS]
Referências encontradas : 335 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 34 ir para página                         

  1 / 335 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28654152
[Au] Autor:Bateman NW; Dubil EA; Wang G; Hood BL; Oliver JM; Litzi TA; Gist GD; Mitchell DA; Blanton B; Phippen NT; Tian C; Zahn CM; Cohn DE; Havrilesky LJ; Berchuck A; Shriver CD; Darcy KM; Hamilton CA; Conrads TP; Maxwell GL
[Ad] Endereço:Gynecologic Cancer Center of Excellence, Department of Obstetrics and Gynecology, Uniformed Services University and Walter Reed National Military Medical Center, Bethesda, Maryland.
[Ti] Título:Race-specific molecular alterations correlate with differential outcomes for black and white endometrioid endometrial cancer patients.
[So] Source:Cancer;123(20):4004-4012, 2017 Oct 15.
[Is] ISSN:1097-0142
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The objective of this study was to identify molecular alterations associated with disease outcomes for white and black patients with endometrioid endometrial cancer (EEC). METHODS: EEC samples from black (n = 17) and white patients (n = 13) were analyzed by proteomics (liquid chromatography-tandem mass spectrometry) and transcriptomics (RNA-seq). Coordinate alterations were validated with RNA-seq data from black (n = 49) and white patients (n = 216). Concordantly altered candidates were further tested for associations with race-specific progression-free survival (PFS) in black (n = 64) or white patients (n = 267) via univariate and multivariate Cox regression modeling and log-rank testing. RESULTS: Discovery analyses revealed significantly altered candidate proteins and transcripts between black and white patients, suggesting modulation of tumor cell viability in black patients and cell death signaling in black and white patients. Eighty-nine candidates were validated as altered between these patient cohorts, and a subset significantly correlated with differential PFS. White-specific PFS candidates included serpin family A member 4 (SERPINA4; hazard ratio [HR], 0.89; Wald P value = .02), integrin subunit α3 (ITGA3; HR, 0.76; P = .03), and Bet1 Golgi vesicular membrane trafficking protein like (BET1L; HR, 0.48; P = .04). Black-specific PFS candidates included family with sequence similarity 228 member B (FAM228B; HR, 0.13; P = .001) and HEAT repeat containing 6 (HEATR6; HR, 4.94; P = .047). Several candidates were also associated with overall survival (SERPINA4 and ITGA3) as well as PFS independent of disease stage, grade and myometrial invasion (SERPINA4, BET1L and FAM228B). CONCLUSIONS: This study has identified and validated molecular alterations in tumors from black and white EEC patients, including candidates significantly associated with altered disease outcomes within these patient cohorts. Cancer 2017;123:4004-12. © 2017 American Cancer Society.
[Mh] Termos MeSH primário: Carcinoma Endometrioide/genética
Neoplasias do Endométrio/genética
[Mh] Termos MeSH secundário: Afroamericanos
Carcinoma Endometrioide/etnologia
Carcinoma Endometrioide/metabolismo
Carcinoma Endometrioide/patologia
Cromatografia Líquida
Intervalo Livre de Doença
Neoplasias do Endométrio/etnologia
Neoplasias do Endométrio/metabolismo
Neoplasias do Endométrio/patologia
Grupo com Ancestrais do Continente Europeu
Feminino
Perfilação da Expressão Gênica
Disparidades nos Níveis de Saúde
Seres Humanos
Integrina alfa3
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Análise Multivariada
Gradação de Tumores
Estadiamento de Neoplasias
Prognóstico
Modelos de Riscos Proporcionais
Proteínas Qc-SNARE
Serpinas
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BET1L protein, human); 0 (ITGA3 protein, human); 0 (Integrin alpha3); 0 (Membrane Proteins); 0 (Qc-SNARE Proteins); 0 (Serpins); 0 (kallistatin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.1002/cncr.30813


  2 / 335 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28618934
[Au] Autor:Li H; Wu H; Zhang H; Li Y; Li S; Hou Q; Wu S; Yang SY
[Ad] Endereço:1 Department of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
[Ti] Título:Identification of curcumin-inhibited extracellular matrix receptors in non-small cell lung cancer A549 cells by RNA sequencing.
[So] Source:Tumour Biol;39(6):1010428317705334, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Curcumin is a potent anti-cancer drug in several types of human cancers. Despite of several preclinical and clinical studies of curcumin, the precise mechanism of curcumin in cancer prevention has remained unclear. In our study, we for the first time investigated whole transcriptome alteration in A549 non-small cell lung cancer (NSCLC) cell lines after treatment with curcumin using RNA sequencing. We found that lots of genes and signaling pathways were significantly altered after curcumin treatment in A549 cells. With bioinformatics approaches (gene ontology, Kyoto Encyclopedia of Genes and Genomes, and STRING), we found that those curcumin altered genes were not only the genes that induce cell death but also those extracellular matrix receptors and mitogen-activated protein kinase signaling pathway genes which regulate cell migration and proliferation. Among those significantly altered genes, eight genes ( COL1A1, COL4A1, COL5A1, LAMA5, ITGA3, ITGA2B, DDIT3, and DUSP1) were further examined by quantitative reverse transcription polymerase chain reaction and western blot analysis in four non-small cell lung cancer cell lines. Both in cell lines and in mouse model, the extracellular matrix receptors including the integrin ( ITGA3 and ITGA2B), collagen ( COL5A1), and laminin ( LAMA5) were significantly inhibited by curcumin at messenger RNA and protein levels. Functional studies confirmed that curcumin not only induced A549 cell death but also repressed cell proliferation and migration by regulating extracellular matrix receptors. Collectively, our study suggests that curcumin may be used as a promising drug candidate for intervening lung cancer in future studies.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Colágeno Tipo V/biossíntese
Curcumina/administração & dosagem
Integrina alfa2/biossíntese
Integrina alfa3/biossíntese
Laminina/biossíntese
[Mh] Termos MeSH secundário: Células A549
Animais
Apoptose/efeitos dos fármacos
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Colágeno Tipo V/genética
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Integrina alfa2/genética
Integrina alfa3/genética
Laminina/genética
Camundongos
RNA Mensageiro/biossíntese
Receptores de Superfície Celular/antagonistas & inibidores
Receptores de Superfície Celular/genética
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (COL5A1 protein, human); 0 (Collagen Type V); 0 (ITGA2B protein, human); 0 (ITGA3 protein, human); 0 (Integrin alpha2); 0 (Integrin alpha3); 0 (Laminin); 0 (RNA, Messenger); 0 (Receptors, Cell Surface); 0 (extracellular matrix receptor); 0 (laminin alpha5); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317705334


  3 / 335 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28612520
[Au] Autor:Koshizuka K; Hanazawa T; Kikkawa N; Arai T; Okato A; Kurozumi A; Kato M; Katada K; Okamoto Y; Seki N
[Ad] Endereço:Department of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.
[Ti] Título:Regulation of ITGA3 by the anti-tumor miR-199 family inhibits cancer cell migration and invasion in head and neck cancer.
[So] Source:Cancer Sci;108(8):1681-1692, 2017 Aug.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:For patients with head and neck squamous cell carcinoma (HNSCC), survival rates have not improved due to local recurrence and distant metastasis. Current targeted molecular therapies do not substantially benefit HNSCC patients. Therefore, it is necessary to use advanced genomic approaches to elucidate the molecular mechanisms underlying the aggressiveness of HNSCC cells. Analysis of our microRNA (miRNA) expression signature by RNA sequencing showed that the miR-199 family (miR-199a-5p, miR-199a-3p, miR-199b-5p and miR-199b-3p) was significantly reduced in cancer tissues. Ectopic expression of mature miRNA demonstrated that all members of the miR-199 family inhibited cancer cell migration and invasion by HNSCC cell lines (SAS and HSC3). These findings suggested that both passenger strands and guide strands of miRNA are involved in cancer pathogenesis. In silico database and genome-wide gene expression analyses revealed that the gene coding for integrin α3 (ITGA3) was regulated by all members of the miR-199 family in HNSCC cells. Knockdown of ITGA3 significantly inhibited cancer cell migration and invasion by HNSCC cells. Moreover, overexpression of ITGA3 was confirmed in HNSCC specimens, and high expression of ITGA3 predicted poorer survival of the patients (P = 0.0048). Our data revealed that both strands of pre-miR-199a (miR-199a-5p and miR-199a-3p) and pre-miR-199b (miR-199b-5p and miR-199b-3p) acted as anti-tumor miRNA in HNSCC cells. Importantly, the involvement of passenger strand miRNA in the regulation of cellular processes is a novel concept in RNA research. Novel miRNA-based approaches for HNSCC can be used to identify potential targets for the development of new therapeutic strategies.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/genética
Neoplasias de Cabeça e Pescoço/genética
Integrina alfa3/genética
MicroRNAs/genética
Análise de Sequência de RNA/métodos
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Adulto
Idoso
Idoso de 80 Anos ou mais
Linhagem Celular Tumoral
Movimento Celular
Simulação por Computador
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Meia-Idade
Invasividade Neoplásica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (ITGA3 protein, human); 0 (Integrin alpha3); 0 (MicroRNAs); 0 (mirn199 microRNA, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13298


  4 / 335 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28324890
[Au] Autor:Sakaguchi T; Yoshino H; Yonemori M; Miyamoto K; Sugita S; Matsushita R; Itesako T; Tatarano S; Nakagawa M; Enokida H
[Ad] Endereço:Department of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan.
[Ti] Título:Regulation of ITGA3 by the dual-stranded microRNA-199 family as a potential prognostic marker in bladder cancer.
[So] Source:Br J Cancer;116(8):1077-1087, 2017 Apr 11.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Based on the microRNA (miRNA) signature of bladder cancer (BC) by deep sequencing, we recently found that several double-stranded mature miRNAs derived from the same pre-miRNAs were sufficiently expressed and acted as tumour suppressors by regulating common target genes in BC. Our deep-sequencing signature of BC showed that all miR-199 family members (miR-199a-3p/-5p and miR-199b-3p/-5p) were also downregulated. We hypothesised that these miRNAs may function as tumour suppressors by regulating common target genes. METHODS: Functional assays of BC cells were performed using transfection of mature miRNA. In silico analyses and luciferase reporter analyses were applied to identify target genes of these miRNAs. The overall survival of patients with BC in The Cancer Genome Atlas (TCGA) database was evaluated by the Kaplan-Meier method. RESULTS: Restoration of these miRNAs significantly inhibited cell migration and invasion in BC cells. Integrin α3 (ITGA3) was directly regulated by these miRNAs. The Cancer Genome Atlas database showed that patients with low pre-miR-199 family (miR-199a-1/-2 and miR-199b) expression exhibited significantly poorer overall survival compared with patients with high pre-miR-199 family expression. CONCLUSIONS: miR-199 family miRNAs functioned as tumour suppressors in BC cells by targeting ITGA3 and might be good prognostic markers for predicting survival in patients with BC.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Integrina alfa3/metabolismo
MicroRNAs/genética
Neoplasias da Bexiga Urinária/genética
[Mh] Termos MeSH secundário: Apoptose
Biomarcadores Tumorais
Western Blotting
Movimento Celular
Proliferação Celular
Seres Humanos
Técnicas Imunoenzimáticas
Integrina alfa3/genética
Estadiamento de Neoplasias
Prognóstico
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Células Tumorais Cultivadas
Neoplasias da Bexiga Urinária/metabolismo
Neoplasias da Bexiga Urinária/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (ITGA3 protein, human); 0 (Integrin alpha3); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (mirn199 microRNA, human)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.43


  5 / 335 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28102841
[Au] Autor:Tang XR; Wen X; He QM; Li YQ; Ren XY; Yang XJ; Zhang J; Wang YQ; Ma J; Liu N
[Ad] Endereço:Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, 651 Dongfeng Road East, Guangzhou, People's Republic of China.
[Ti] Título:MicroRNA-101 inhibits invasion and angiogenesis through targeting ITGA3 and its systemic delivery inhibits lung metastasis in nasopharyngeal carcinoma.
[So] Source:Cell Death Dis;8(1):e2566, 2017 Jan 19.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Clinically, distant metastasis after primary treatment remains a key problem in nasopharyngeal carcinoma (NPC), and the treatment outcome of metastatic NPC remains disappointing, so there is a pressing need to identify novel therapeutic strategies. In accordance with our previous microarray data, we found that miR-101 was downregulated in NPC clinical specimens and cell lines. Ectopic expression of miR-101 significantly suppressed NPC cell migration, invasion and angiogenesis in vitro and inhibited angiogenesis and metastasis in vivo using the chicken chorioallantoic membrane model. Furthermore, ITGA3 was identified and validated as a novel target of miR-101, and the restoration of ITGA3 expression potently rescued the suppressive effects of miR-101. In addition, NPC patients with high ITGA3 expression had poorer overall survival and distant metastasis-free survival than patients with low ITGA3 expression, and ITGA3 overexpression was an independent poor prognostic factor in NPC. More importantly, we demonstrated that the systemic delivery of lentivirus-mediated miR-101 abrogated the lung metastatic colonization formation of NPC cells without obvious toxicity. Our study elucidates the molecular mechanisms of miR-101/ITGA3 pathway in regulating NPC metastasis and angiogenesis, and the systemic delivery of miR-101 provides a potent evidence for the development of a novel microRNA-targeting anticancer strategy for NPC patients.
[Mh] Termos MeSH primário: Carcinoma/genética
Integrina alfa3/genética
Neoplasias Pulmonares/genética
MicroRNAs/genética
Neoplasias Nasofaríngeas/genética
Neovascularização Patológica/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Carcinoma/patologia
Carcinoma/terapia
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Neoplasias Pulmonares/patologia
Neoplasias Pulmonares/secundário
Neoplasias Pulmonares/terapia
Masculino
Camundongos
MicroRNAs/biossíntese
MicroRNAs/uso terapêutico
Meia-Idade
Neoplasias Nasofaríngeas/patologia
Neoplasias Nasofaríngeas/terapia
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Neovascularização Patológica/patologia
Neovascularização Patológica/terapia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ITGA3 protein, human); 0 (Integrin alpha3); 0 (MIRN101 microRNA, human); 0 (MicroRNAs)
[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:170120
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2016.486


  6 / 335 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27639064
[Au] Autor:Azzariti A; Mancarella S; Porcelli L; Quatrale AE; Caligiuri A; Lupo L; Dituri F; Giannelli G
[Ad] Endereço:National Cancer Institute, Istituto Tumori G. Paolo II, Bari, Italy.
[Ti] Título:Hepatic stellate cells induce hepatocellular carcinoma cell resistance to sorafenib through the laminin-332/α3 integrin axis recovery of focal adhesion kinase ubiquitination.
[So] Source:Hepatology;64(6):2103-2117, 2016 Dec.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In patients with hepatocellular carcinoma (HCC) receiving sorafenib, drug resistance is common. HCC develops in a microenvironment enriched with extracellular matrix proteins including laminin (Ln)-332, produced by hepatic stellate cells (HSCs). Ln-332 is the ligand of α3ß1 and α6ß4 integrins, differently expressed on the HCC cell surface, that deliver intracellular pathways. The aim of this study was to investigate the effect of Ln-332 on sorafenib's effectiveness. HCC cells were challenged with sorafenib in the presence of Ln-332 and of HSC conditioned medium (CM). Sorafenib impaired HCC cell proliferation and induced apoptosis. HSC-CM or Ln-332 inhibited sorafenib's effectiveness in HCC cells expressing both α3ß1 and α6ß4. Inhibiting α3 but not α6 integrin subunit using blocking antibodies or small interfering RNA abrogated the protection induced by Ln-332 and HSC-CM. Hep3B cells expressing α6ß4 but lacking the α3 integrin were insensitive to Ln-332 and HSC-CM protective effects. Hep3B α3-positive, but not wild-type and scramble transfected, cells acquired protection by sorafenib when plated on Ln-332-CM or HSCs. Sorafenib dephosphorylated focal adhesion kinase (FAK) and extracellular signal-regulated kinases 1/2, whereas Ln-332 and HSC-CM partially restored the pathways. Silencing FAK, but not extracellular signal-regulated kinases 1/2, abrogated the protection induced by Ln-332 and HSC-CM, suggesting a specific role for FAK. Sorafenib down-regulated total FAK, inducing its proteasomal degradation, while Ln-332 and HSC-CM promoted the escape of FAK from ubiquitination, probably inducing a preferential membrane localization. CONCLUSION: This study unveils a novel mechanism of sorafenib resistance depending on the α3ß1/Ln-332 axis and requiring FAK ubiquitination, providing new insights into personalizing therapy for patients with HCC. (Hepatology 2016;64:2103-2117).
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Carcinoma Hepatocelular/tratamento farmacológico
Resistência a Medicamentos Antineoplásicos
Proteína-Tirosina Quinases de Adesão Focal/fisiologia
Células Estreladas do Fígado/fisiologia
Integrina alfa3/fisiologia
Laminina/fisiologia
Neoplasias Hepáticas/tratamento farmacológico
Niacinamida/análogos & derivados
Compostos de Fenilureia/uso terapêutico
Ubiquitinação
[Mh] Termos MeSH secundário: Seres Humanos
Niacinamida/uso terapêutico
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Integrin alpha3); 0 (Laminin); 0 (Phenylurea Compounds); 25X51I8RD4 (Niacinamide); 9ZOQ3TZI87 (sorafenib); EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160918
[St] Status:MEDLINE
[do] DOI:10.1002/hep.28835


  7 / 335 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27310876
[Au] Autor:Liu CC; Leclair P; Monajemi M; Sly LM; Reid GS; Lim CJ
[Ad] Endereço:Department of Pediatrics, University of British Columbia, Vancouver, BC, Canada V5Z 4H4.
[Ti] Título:α-Integrin expression and function modulates presentation of cell surface calreticulin.
[So] Source:Cell Death Dis;7:e2268, 2016 Jun 16.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Calreticulin presentation on the cell surface is an important hallmark of immunogenic cell death (ICD), serving as the prophagocytic signal for macrophages. Cell adhesion is a physiologically relevant stimulus previously shown to increase calreticulin interaction with α-integrins via the juxtamembrane, cytosolic GFFKR motif. This study assessed whether integrin function can regulate surface calreticulin levels in ICD. We generated calreticulin-null T-lymphoblasts and confirmed the loss of surface calreticulin expression on cells treated with doxorubicin, an ICD inducer. Reconstituted expression with full-length calreticulin targeted to the endoplasmic reticulum (ER) successfully rescued doxorubicin-induced surface calreticulin. Reconstitution with a truncation mutant calreticulin targeted to the cytosol led to constitutively high surface calreticulin that was not further elevated by doxorubicin, suggesting calreticulin released from the stressed ER transits the cytosol before its translocation to the cell surface. When stimulated to engage integrin substrates, doxorubicin-treated wild-type T-lymphoblasts exhibited decreased surface calreticulin compared with cells under non-adherent conditions. The inhibitory effect on surface calreticulin was recapitulated for cells in suspension treated with a ß1-integrin-activating antibody, 9EG7. Similarly, cells expressing a truncated α-integrin cytosolic tail, bearing only the juxtamembrane GFFKR calreticulin-binding motif, exhibited low surface calreticulin with doxorubicin treatment under non-adherent conditions. Using partial permeabilization techniques to distinguish between cytosolic and ER staining, we found that ICD inducers promoted the accumulation of cytosolic calreticulin with negligible change in total calreticulin, suggesting that integrin-mediated inhibition of surface calreticulin was due to reduced cytosolic to surface translocation. T-lymphoblasts co-treated with an ICD inducer and 9EG7 exhibited reduced phagocytosis by macrophages when compared with treatment with only ICD inducer. This study reveals a previously uncharacterized function of integrins as negative regulators of ICD by suppressing presentation of cell surface calreticulin.
[Mh] Termos MeSH primário: Calreticulina/genética
Regulação Leucêmica da Expressão Gênica
Integrina alfa3/genética
Integrina alfa4/genética
Integrina alfa5/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Antibióticos Antineoplásicos/farmacologia
Anticorpos/farmacologia
Sequência de Bases
Calreticulina/imunologia
Linhagem Celular Tumoral
Técnicas de Cocultura
Doxorrubicina/farmacologia
Retículo Endoplasmático/efeitos dos fármacos
Retículo Endoplasmático/metabolismo
Seres Humanos
Integrina alfa3/imunologia
Integrina alfa4/imunologia
Integrina alfa5/imunologia
Integrina beta1/genética
Integrina beta1/imunologia
Células Jurkat
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Macrófagos/patologia
Leucemia-Linfoma Linfoblástico de Células Precursoras/imunologia
Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia
Cultura Primária de Células
Transporte Proteico
Transdução de Sinais
Linfócitos T/efeitos dos fármacos
Linfócitos T/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 0 (Antibodies); 0 (Calreticulin); 0 (Integrin alpha3); 0 (Integrin alpha5); 0 (Integrin beta1); 0 (calreticulin, human); 143198-26-9 (Integrin alpha4); 80168379AG (Doxorubicin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160617
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2016.176


  8 / 335 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26992919
[Au] Autor:Tilghman J; Schiapparelli P; Lal B; Ying M; Quinones-Hinojosa A; Xia S; Laterra J
[Ad] Endereço:Hugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD, 21205, USA; Department of Neuroscience, Johns Hopkins School of Medicine, Baltimore, MD, 21205, USA.
[Ti] Título:Regulation of Glioblastoma Tumor-Propagating Cells by the Integrin Partner Tetraspanin CD151.
[So] Source:Neoplasia;18(3):185-98, 2016 Mar.
[Is] ISSN:1476-5586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma (GBM) stem cells (GSCs) represent tumor-propagating cells with stem-like characteristics (stemness) that contribute disproportionately to GBM drug resistance and tumor recurrence. Understanding the mechanisms supporting GSC stemness is important for developing therapeutic strategies for targeting GSC-dependent oncogenic mechanisms. Using GBM-derived neurospheres, we identified the cell surface tetraspanin family member CD151 as a novel regulator of glioma cell stemness, GSC self-renewal capacity, migration, and tumor growth. CD151 was found to be overexpressed in GBM tumors and GBM neurospheres enriched in GSCs. Silencing CD151 inhibited neurosphere forming capacity, neurosphere cell proliferation, and migration and attenuated the expression of markers and transcriptional drivers of the GSC phenotype. Conversely, forced CD151 expression promoted neurosphere self-renewal, cell migration, and expression of stemness-associated transcription factors. CD151 was found to complex with integrins α3, α6, and ß1 in neurosphere cells, and blocking CD151 interactions with integrins α3 and α6 inhibited AKT phosphorylation, a downstream effector of integrin signaling, and impaired sphere formation and neurosphere cell migration. Additionally, targeting CD151 in vivo inhibited the growth of GBM neurosphere-derived xenografts. These findings identify CD151 and its interactions with integrins α3 and α6 as potential therapeutic targets for inhibiting stemness-driving mechanisms and stem cell populations in GBM.
[Mh] Termos MeSH primário: Glioblastoma/genética
Integrina alfa3/genética
Integrina alfa6/genética
Tetraspanina 24/biossíntese
[Mh] Termos MeSH secundário: Carcinogênese/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Regulação Neoplásica da Expressão Gênica
Glioblastoma/patologia
Seres Humanos
Células-Tronco Neoplásicas
Tetraspanina 24/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (CD151 protein, human); 0 (ITGA3 protein, human); 0 (ITGA6 protein, human); 0 (Integrin alpha3); 0 (Integrin alpha6); 0 (Tetraspanin 24)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160320
[St] Status:MEDLINE


  9 / 335 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26906622
[Au] Autor:Du J; Liu X; Wu Y; Zhu J; Tang Y
[Ad] Endereço:Department of Cardiothoracic Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China; Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210028, China.
[Ti] Título:Essential role of STX6 in esophageal squamous cell carcinoma growth and migration.
[So] Source:Biochem Biophys Res Commun;472(1):60-7, 2016 Mar 25.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Abnormalities in endosomes, or dysregulation in their trafficking, play an important role directly in many diseases including oncogenesis. Syntaxin-6 (STX6) is involved in diverse cellular functions in a variety of cell types and has been shown to regulate many intracellular membrane trafficking events such as endocytosis, recycling and anterograde and retrograde trafficking. However, its expression pattern and biological functions in esophageal squamous cell carcinoma (ESCC) remained unknown. Here, we have found that the expression of STX6 was up-regulated in ESCC samples, its expression was significantly correlated with tumor size, histological differentiation, lymph node metastasis and depth. On one hand, STX6 silencing inhibited ESCC cells viability and proliferation in a p53-dependent manner. On the other hand, STX6 effect integrin trafficking and regulate ESCC cells migration. Taken together, our study revealed the oncogenic roles of STX6 in the progression of ESCC, and it might be a valuable target for ESCC therapy.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/metabolismo
Neoplasias Esofágicas/metabolismo
Proteínas Qa-SNARE/metabolismo
[Mh] Termos MeSH secundário: Idoso
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/patologia
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Sobrevivência Celular
Neoplasias Esofágicas/genética
Neoplasias Esofágicas/patologia
Feminino
Técnicas de Silenciamento de Genes
Seres Humanos
Imuno-Histoquímica
Integrina alfa3/metabolismo
Masculino
Meia-Idade
Proteínas Qa-SNARE/antagonistas & inibidores
Proteínas Qa-SNARE/genética
RNA Interferente Pequeno/genética
Proteína Supressora de Tumor p53/antagonistas & inibidores
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Integrin alpha3); 0 (Qa-SNARE Proteins); 0 (RNA, Small Interfering); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160316
[Lr] Data última revisão:
160316
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160225
[St] Status:MEDLINE


  10 / 335 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26800307
[Au] Autor:Escate R; Padro T; Badimon L
[Ad] Endereço:Cardiovascular Research Center (CSIC-ICCC), IIB-Sant Pau, Barcelona, Spain.
[Ti] Título:LDL accelerates monocyte to macrophage differentiation: Effects on adhesion and anoikis.
[So] Source:Atherosclerosis;246:177-86, 2016 Mar.
[Is] ISSN:1879-1484
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: High LDL triggers dyslipidemia and atherosclerosis, a chronic inflammatory disease with participation of the innate immunity system. Monocytes are recruited to areas of LDL-induced endothelial damage and initiate differentiation. This study was aimed to investigate the effects of LDL on the early transitional stages of monocyte differentiation into macrophages. METHODS: Blood monocytes, isolated from healthy donors by their adhesion properties, were exposed to native-LDL (1.80 mg/mL) for 48-h. Monocyte phenotype was assessed at transcript and miRNA levels by real-time PCR. Protein-expression was determined by western-blot and flow-cytometry. RESULTS: CD14 time-dependently decreased in adhered monocytes, reaching a >4 fold decrease at transcript- and protein-levels after 7-days in culture when cells were already differentiated into macrophages. At 4-days differentiation, monocytes exposed to LDL reduced CD14-transcrition >1.5 fold in mRNA (p = 0.002) and 34% CD14-protein (p = 0.039), whereas increased in CD16-expression (p = 0.019). Besides, LDL induced a significant increase in integrin CD49c (α3-subunit) at mRNA (>2 fold, p = 0.008) and protein (>3 fold, p = 0.045) level and a decrease in the apoptosis-effectors CASP8 and CASP3 (p = 0.002 and p = 0.035, respectively) as well as in the precursor form of the death-receptor DR5 (p = 0.045) without affecting its mRNA-expression level, suggesting a LDL-dependent post-transcriptional regulation of DR5. In silico prediction analysis indicated miR-126-3p as a candidate to regulate DR5-expression and miR-126-3p was shown affected by LDL reaching a significant increase (p = 0.033). CONCLUSIONS: In differentiating human monocytes, LDL stimulates expression of cell-adhesion molecules and downregulates apoptosis-effectors, regulating anoikis and survival programs in the early stage macrophages.
[Mh] Termos MeSH primário: Anoikis/efeitos dos fármacos
Adesão Celular/efeitos dos fármacos
Transdiferenciação Celular/efeitos dos fármacos
Lipoproteínas LDL/farmacologia
Macrófagos/efeitos dos fármacos
Monócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Moléculas de Adesão Celular/genética
Moléculas de Adesão Celular/metabolismo
Células Cultivadas
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/metabolismo
Seres Humanos
Integrina alfa3/genética
Integrina alfa3/metabolismo
Receptores de Lipopolissacarídeos/genética
Receptores de Lipopolissacarídeos/metabolismo
Macrófagos/metabolismo
Macrófagos/patologia
MicroRNAs/genética
MicroRNAs/metabolismo
Monócitos/metabolismo
Monócitos/patologia
Fenótipo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores de IgG/genética
Receptores de IgG/metabolismo
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Fatores de Tempo
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (Integrin alpha3); 0 (Lipopolysaccharide Receptors); 0 (Lipoproteins, LDL); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (Receptors, IgG); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (TNFRSF10B protein, human)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160123
[St] Status:MEDLINE



página 1 de 34 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