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Pesquisa : D08.811.464.938.750.210.250 [Categoria DeCS]
Referências encontradas : 263 [refinar]
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[PMID]:28582465
[Au] Autor:Qattan MY; Bakker EY; Rajendran R; Chen DW; Saha V; Liu J; Zeef L; Schwartz JM; Mutti L; Demonacos C; Krstic-Demonacos M
[Ad] Endereço:College of Applied Medical Sciences and Community Services (CAMS&CS), King Saud University, Riyadh, Saudi Arabia.
[Ti] Título:Differential regulation of cell death pathways by the microenvironment correlates with chemoresistance and survival in leukaemia.
[So] Source:PLoS One;12(6):e0178606, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glucocorticoids (GCs) and topoisomerase II inhibitors are used to treat acute lymphoblastic leukaemia (ALL) as they induce death in lymphoid cells through the glucocorticoid receptor (GR) and p53 respectively. Mechanisms underlying ALL cell death and the contribution of the bone marrow microenvironment to drug response/resistance remain unclear. The role of the microenvironment and the identification of chemoresistance determinants were studied by transcriptomic analysis in ALL cells treated with Dexamethasone (Dex), and Etoposide (Etop) grown in the presence or absence of bone marrow conditioned media (CM). The necroptotic (RIPK1) and the apoptotic (caspase-8/3) markers were downregulated by CM, whereas the inhibitory effects of chemotherapy on the autophagy marker Beclin-1 (BECN1) were reduced suggesting CM exerts cytoprotective effects. GCs upregulated the RIPK1 ubiquitinating factor BIRC3 (cIAP2), in GC-sensitive (CEM-C7-14) but not in resistant (CEM-C1-15) cells. In addition, CM selectively affected GR phosphorylation in a site and cell-specific manner. GR is recruited to RIPK1, BECN1 and BIRC3 promoters in the sensitive but not in the resistant cells with phosphorylated GR forms being generally less recruited in the presence of hormone. FACS analysis and caspase-8 assays demonstrated that CM promoted a pro-survival trend. High molecular weight proteins reacting with the RIPK1 antibody were modified upon incubation with the BIRC3 inhibitor AT406 in CEM-C7-14 cells suggesting that they represent ubiquitinated forms of RIPK1. Our data suggest that there is a correlation between microenvironment-induced ALL proliferation and altered response to chemotherapy.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Resistência a Medicamentos Antineoplásicos/genética
Regulação Neoplásica da Expressão Gênica
Glucocorticoides/farmacologia
Inibidores da Topoisomerase II/farmacologia
Microambiente Tumoral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Azocinas/farmacologia
Proteína 3 com Repetições IAP de Baculovírus
Beclina-1/genética
Beclina-1/metabolismo
Compostos Benzidrílicos/farmacologia
Células da Medula Óssea/patologia
Células da Medula Óssea/secreção
Caspase 3/genética
Caspase 3/metabolismo
Caspase 8/genética
Caspase 8/metabolismo
Linhagem Celular
Linhagem Celular Tumoral
Meios de Cultivo Condicionados/farmacologia
Dexametasona/farmacologia
Etoposídeo/farmacologia
Seres Humanos
Proteínas Inibidoras de Apoptose/antagonistas & inibidores
Proteínas Inibidoras de Apoptose/genética
Proteínas Inibidoras de Apoptose/metabolismo
Células K562
Necrose/induzido quimicamente
Necrose/genética
Necrose/metabolismo
Necrose/patologia
Fosforilação/efeitos dos fármacos
Proteína Serina-Treonina Quinases de Interação com Receptores/genética
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Receptores de Glucocorticoides/antagonistas & inibidores
Receptores de Glucocorticoides/genética
Receptores de Glucocorticoides/metabolismo
Transdução de Sinais
Transcriptoma
Microambiente Tumoral/genética
Ubiquitina-Proteína Ligases/antagonistas & inibidores
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Azocines); 0 (BECN1 protein, human); 0 (Beclin-1); 0 (Benzhydryl Compounds); 0 (Culture Media, Conditioned); 0 (Glucocorticoids); 0 (Inhibitor of Apoptosis Proteins); 0 (N-benzhydryl-5-(2-(methylamino)propanamido)-3-(3-methylbutanoyl)-6-oxodecahydropyrrolo(1,2-a)(1,5)diazocine-8-carboxamide); 0 (Receptors, Glucocorticoid); 0 (Topoisomerase II Inhibitors); 6PLQ3CP4P3 (Etoposide); 7S5I7G3JQL (Dexamethasone); EC 2.3.2.27 (BIRC3 protein, human); EC 2.3.2.27 (Baculoviral IAP Repeat-Containing 3 Protein); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.1 (RIPK1 protein, human); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (CASP8 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 8)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178606


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[PMID]:28425584
[Au] Autor:Hay-Koren A; Bialik S; Levin-Salomon V; Kimchi A
[Ad] Endereço:Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
[Ti] Título:Changes in cIAP2, survivin and BimEL expression characterize the switch from autophagy to apoptosis in prolonged starvation.
[So] Source:J Intern Med;281(5):458-470, 2017 May.
[Is] ISSN:1365-2796
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Autophagy is a catabolic process involving the engulfment of cytoplasmic content within autophagosomes followed by their delivery to lysosomes. This process is a survival mechanism, enabling cells to cope with nutrient deprivation by degradation and recycling of macromolecules. Yet during continued stress such as prolonged starvation, a switch from autophagy to apoptosis is often detected. OBJECTIVE: In this work, we characterized the temporal dynamics of the transition from autophagy towards apoptosis with the aim of elucidating the molecular mechanism regulating the switch from survival autophagy to apoptotic cell death. RESULTS AND CONCLUSIONS: We defined an inverse relationship between apoptosis and autophagy spanning a period of 72 h, manifested by the sequential reduction in LC3 lipidation and the activation of caspase-3. The transition to apoptosis correlated with a selective decline in the mRNA and protein levels of two anti-apoptotic IAP family proteins, survivin and cIAP2 and a selective increase in the BH3-only protein, BimEL. This 'molecular signature' was common to several cell lines undergoing the switch from autophagy to apoptosis during prolonged starvation. Mechanistically, the increased BimEL protein levels resulted from its reduced binding to its specific E3 ligase, ßTrCP, leading to protein stabilization. Consistent with this, BimEL showed decreased phosphorylation at critical sites previously reported to be essential for binding to the E3 ligase. The decrease in the anti-apoptotic IAPs and the increase in the pro-apoptotic BimEL may thus constitute a molecular switch from autophagy to apoptosis during prolonged starvation.
[Mh] Termos MeSH primário: Apoptose/fisiologia
Autofagia/fisiologia
Proteína 11 Semelhante a Bcl-2/metabolismo
Proteínas Inibidoras de Apoptose/metabolismo
Inanição/fisiopatologia
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Células A549
Proteínas Relacionadas à Autofagia/metabolismo
Proteína 3 com Repetições IAP de Baculovírus
Células Cultivadas
Seres Humanos
Proteínas Contendo Repetições de beta-Transducina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autophagy-Related Proteins); 0 (BCL2L11 protein, human); 0 (BIRC5 protein, human); 0 (BTRC protein, human); 0 (Bcl-2-Like Protein 11); 0 (Inhibitor of Apoptosis Proteins); 0 (beta-Transducin Repeat-Containing Proteins); EC 2.3.2.27 (BIRC3 protein, human); EC 2.3.2.27 (Baculoviral IAP Repeat-Containing 3 Protein); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[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:170421
[St] Status:MEDLINE
[do] DOI:10.1111/joim.12616


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[PMID]:28295868
[Au] Autor:Jiang X; Li C; Lin B; Hong H; Jiang L; Zhu S; Wang X; Tang N; Li X; She F; Chen Y
[Ad] Endereço:Department of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fujian Medical University, Fuzhou, China.
[Ti] Título:cIAP2 promotes gallbladder cancer invasion and lymphangiogenesis by activating the NF-κB pathway.
[So] Source:Cancer Sci;108(6):1144-1156, 2017 Jun.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Several studies have produced contradictory findings about the prognostic implications for inhibitor of apoptosis proteins (IAP) in different types of cancer. Cellular inhibitor of apoptosis 2 (cIAP2/BIRC) is one of the most extensively characterized human IAP. To date, no studies have focused on the expression level of cIAP2 in human gallbladder cancer (GBC), and the mechanism of cIAP2 in GBC invasion and lymphangiogenesis remains unclear. Therefore, in the present study, cIAP2 expression in GBC was detected using quantitative real-time polymerase chain reaction and immunohistochemistry, and the relationship between cIAP2 levels in cancer tissues and the clinicopathological characteristics of patients was analyzed. The biological effect of cIAP2 in GBC cells was tested using the Cell Counting Kit-8 Assay, Transwell assays and the ability of human dermal lymphatic endothelial cells (HDLEC) to undergo tube formation. The role of cIAP2 in activating the NF-κB pathway was determined using a dual-luciferase reporter assay, immunofluorescence staining, western blotting and ELISA. Finally, an animal model was used to further confirm the role of cIAP2 in lymphangiogenesis. We showed that cIAP2 expression was elevated in human GBC tissues and correlated with a negative prognosis for patients. Moreover, cIAP2 was identified as a lymphangiogenic factor of GBC cells and, thus, promoted lymph node metastasis in GBC cells. Our study is the first to suggest that cIAP2 can promote GBC invasion and lymphangiogenesis by activating the NF-κB pathway.
[Mh] Termos MeSH primário: Neoplasias da Vesícula Biliar/genética
Neoplasias da Vesícula Biliar/patologia
Proteínas Inibidoras de Apoptose/genética
Linfangiogênese/genética
NF-kappa B/genética
Transdução de Sinais/genética
Ubiquitina-Proteína Ligases/genética
[Mh] Termos MeSH secundário: Idoso
Animais
Proteína 3 com Repetições IAP de Baculovírus
Linhagem Celular
Linhagem Celular Tumoral
Proliferação Celular/genética
Feminino
Regulação Neoplásica da Expressão Gênica/genética
Seres Humanos
Metástase Linfática/genética
Metástase Linfática/patologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inhibitor of Apoptosis Proteins); 0 (NF-kappa B); EC 2.3.2.27 (BIRC3 protein, human); EC 2.3.2.27 (Baculoviral IAP Repeat-Containing 3 Protein); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13236


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[PMID]:28093282
[Au] Autor:Mendoza-Rodríguez M; Arévalo Romero H; Fuentes-Pananá EM; Ayala-Sumuano JT; Meza I
[Ad] Endereço:Departamento de Biomedicina Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Avenida Instituto Politécnico Nacional 2508, San Pedro Zacatenco, Ciudad de México 07360, Mexico.
[Ti] Título:IL-1ß induces up-regulation of BIRC3, a gene involved in chemoresistance to doxorubicin in breast cancer cells.
[So] Source:Cancer Lett;390:39-44, 2017 Apr 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Epithelial to mesenchymal transition (EMT) of tumor cells facilitates their progress to metastasis. In the tumor microenvironment the inflammatory cytokine 1ß (IL-1ß) has been associated with tumor development and invasiveness. IL-1ß-induced EMT triggers the expression of markers associated with malignancy. We have recently reported that an IL-1ß-highly responsive clone (6D cells) from non-invasive MCF-7 breast cancer cells activates PI3K/Rac and IL-1RI/ß-catenin pathways that up-regulate the transcription of genes involved in an EMT-like process. However, a correlation between the EMT program induced by a pro-inflammatory environment, and the acquisition of chemoresistance has not been yet determined in these cells. In this work, we report the expression of cell survival genes after IL-1ß stimulation of 6D cells. The expression of CDKN1A, TP63, SFN and, particularly, BIRC3 was found to be up-regulated in a RNA-seq analysis and validated by qPCR. Cells stimulated with IL-1ß when challenged with doxorubicin showed resistance to the drug, whereas silencing of BIRC3 decreased viability of the cells treated with the drug. Our present results show that IL-1ß confers doxorubicin resistance to breast cancer cells, underlining the importance of an inflammatory environment in cancer malignancy.
[Mh] Termos MeSH primário: Neoplasias da Mama/tratamento farmacológico
Neoplasias da Mama/fisiopatologia
Doxorrubicina/uso terapêutico
Resistência a Medicamentos Antineoplásicos/genética
Proteínas Inibidoras de Apoptose/genética
Interleucina-1beta/farmacologia
Ubiquitina-Proteína Ligases/genética
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Proteína 3 com Repetições IAP de Baculovírus
Western Blotting
Neoplasias da Mama/metabolismo
Linhagem Celular Tumoral
Feminino
Seres Humanos
Interleucina-1beta/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inhibitor of Apoptosis Proteins); 0 (Interleukin-1beta); 80168379AG (Doxorubicin); EC 2.3.2.27 (BIRC3 protein, human); EC 2.3.2.27 (Baculoviral IAP Repeat-Containing 3 Protein); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[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:170118
[St] Status:MEDLINE


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[PMID]:27889570
[Au] Autor:Grabinger T; Bode KJ; Demgenski J; Seitz C; Delgado ME; Kostadinova F; Reinhold C; Etemadi N; Wilhelm S; Schweinlin M; Hänggi K; Knop J; Hauck C; Walles H; Silke J; Wajant H; Nachbur U; W Wei-Lynn W; Brunner T
[Ad] Endereço:Biochemical Pharmacology, Department of Biology, University of Konstanz, Germany.
[Ti] Título:Inhibitor of Apoptosis Protein-1 Regulates Tumor Necrosis Factor-Mediated Destruction of Intestinal Epithelial Cells.
[So] Source:Gastroenterology;152(4):867-879, 2017 Mar.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Tumor necrosis factor (TNF) is a cytokine that promotes inflammation and contributes to pathogenesis of inflammatory bowel diseases. Unlike other cells and tissues, intestinal epithelial cells undergo rapid cell death upon exposure to TNF, by unclear mechanisms. We investigated the roles of inhibitor of apoptosis proteins (IAPs) in the regulation of TNF-induced cell death in the intestinal epithelium of mice and intestinal organoids. METHODS: RNA from cell lines and tissues was analyzed by quantitative polymerase chain reaction, protein levels were analyzed by immunoblot assays. BIRC2 (also called cIAP1) was expressed upon induction from lentiviral vectors in young adult mouse colon (YAMC) cells. YAMC cells, the mouse colon carcinoma cell line MC38, the mouse macrophage cell line RAW 264.7, or mouse and human organoids were incubated with second mitochondrial activator of caspases (Smac)-mimetic compound LCL161 or recombinant TNF-like weak inducer of apoptosis (TNFSF12) along with TNF, and cell death was quantified. C57BL/6 mice with disruption of Xiap, Birc2 (encodes cIAP1), Birc3 (encodes cIAP2), Tnfrsf1a, or Tnfrsf1b (Tnfrsf1a and b encode TNF receptors) were injected with TNF or saline (control); liver and intestinal tissues were collected and analyzed for apoptosis induction by cleaved caspase 3 immunohistochemistry. We also measured levels of TNF and alanine aminotransferase in serum from mice. RESULTS: YAMC cells, and mouse and human intestinal organoids, died rapidly in response to TNF. YAMC and intestinal crypts expressed lower levels of XIAP, cIAP1, cIAP2, and cFLIP than liver tissue. Smac-mimetics reduced levels of cIAP1 and XIAP in MC38 and YAMC cells, and Smac-mimetics and TNF-related weak inducer of apoptosis increased TNF-induced cell death in YAMC cells and organoids-most likely by sequestering and degrading cIAP1. Injection of TNF greatly increased levels of cell death in intestinal tissue of cIAP1-null mice, compared with wild-type C57BL/6 mice, cIAP2-null mice, or XIAP-null mice. Excessive TNF-induced cell death in the intestinal epithelium was mediated TNF receptor 1. CONCLUSIONS: In a study of mouse and human cell lines, organoids, and tissues, we found cIAP1 to be required for regulation of TNF-induced intestinal epithelial cell death and survival. These findings have important implications for the pathogenesis of TNF-mediated enteropathies and chronic inflammatory diseases of the intestine.
[Mh] Termos MeSH primário: Apoptose
Células Epiteliais
Proteínas Inibidoras de Apoptose/genética
Proteínas Inibidoras de Apoptose/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Apoptose/genética
Proteína 3 com Repetições IAP de Baculovírus
Morte Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Citocina TWEAK
Células Epiteliais/efeitos dos fármacos
Seres Humanos
Mucosa Intestinal/citologia
Mucosa Intestinal/efeitos dos fármacos
Fígado/efeitos dos fármacos
Macrófagos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Organoides
Receptores Tipo I de Fatores de Necrose Tumoral/genética
Receptores Tipo II do Fator de Necrose Tumoral/genética
Tiazóis/farmacologia
Fator de Necrose Tumoral alfa/farmacologia
Fatores de Necrose Tumoral/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Birc4 protein, mouse); 0 (Cytokine TWEAK); 0 (Inhibitor of Apoptosis Proteins); 0 (LCL161); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (TNFSF12 protein, human); 0 (Thiazoles); 0 (Tnfrsf1a protein, mouse); 0 (Tnfsf12 protein, mouse); 0 (Tumor Necrosis Factor-alpha); 0 (Tumor Necrosis Factors); EC 2.3.2.27 (BIRC2 protein, human); EC 2.3.2.27 (Baculoviral IAP Repeat-Containing 3 Protein); EC 2.3.2.27 (Birc2 protein, mouse); EC 2.3.2.27 (Birc3 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161128
[St] Status:MEDLINE


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[PMID]:27304223
[Au] Autor:Roscioli E; Hamon R; Ruffin RE; Grant J; Hodge S; Zalewski P; Lester S
[Ad] Endereço:a Discipline of Medicine, University of Adelaide , North Tce, Adelaide , South Australia , Australia.
[Ti] Título:BIRC3 single nucleotide polymorphism associate with asthma susceptibility and the abundance of eosinophils and neutrophils.
[So] Source:J Asthma;54(2):116-124, 2017 Mar.
[Is] ISSN:1532-4303
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND OBJECTIVE: Aberrant apoptosis is a disease susceptibility mechanism relevant for asthma, whereby fragility of the airway epithelium and enhanced survival of inflammatory cells, contributes to its pathogenesis and prolongation. Cellular Inhibitor of Apoptosis Proteins (cIAP) suppress apoptosis, and participate in the immune response. In this study, single nucleotide polymorphisms (SNP) in the BIRC2 (codes cIAP1) and BIRC3 (cIAP2) genes were evaluated for an association with asthma. METHODS: Caucasian asthmatic (n = 203) and control (n = 198) subjects were selected from participants in the North West Adelaide Health Study. SNPs (n = 9) spanning the consecutively positioned BIRC2 and BIRC3 genes, were selected using a haplotype tagging approach. Alleles and haplotype associations were analysed by logistic regression, assuming an additive genetic model, and adjusted for gender and atopy. RESULTS: The frequency of the minor allele for the BIRC3 SNP rs3460 was significantly lower in asthmatics compared to the control cases (P = 0.046). BIRC3 SNPs rs7928663 and rs7127583 associated with a reduction in eosinophil and neutrophil abundance when assessed across the study population (multivariate P values = 0.002, and 0.005, respectively). Further, the frequency of a haplotype tagged by rs3460, rs7928663 and rs7127583 was reduced in the asthma sub group (P = 0.05), while the presence of the major allele for rs7928663 associated with an increased load of circulating eosinophils and neutrophils (multivariate P value = 0.001). CONCLUSIONS: Polymorphisms in the BIRC3 gene, but not BIRC2, are associated with a protective effect with regards to asthma susceptibility, and a reduced load of inflammatory cells.
[Mh] Termos MeSH primário: Asma/genética
Asma/imunologia
Eosinófilos/metabolismo
Proteínas Inibidoras de Apoptose/genética
Neutrófilos/metabolismo
Ubiquitina-Proteína Ligases/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Alelos
Apoptose/genética
Proteína 3 com Repetições IAP de Baculovírus
Grupo com Ancestrais do Continente Europeu/genética
Feminino
Frequência do Gene
Predisposição Genética para Doença/genética
Genótipo
Haplótipos
Seres Humanos
Contagem de Leucócitos
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inhibitor of Apoptosis Proteins); EC 2.3.2.27 (BIRC2 protein, human); EC 2.3.2.27 (BIRC3 protein, human); EC 2.3.2.27 (Baculoviral IAP Repeat-Containing 3 Protein); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[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:160616
[St] Status:MEDLINE
[do] DOI:10.1080/02770903.2016.1196371


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[PMID]:27282269
[Au] Autor:Yoon H; Kim SG; Kim BK; Shin E; Kim N; Lee HJ; Kang GH; Jung HC
[Ad] Endereço:Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
[Ti] Título: Eradication Downregulates Cellular Inhibitor of Apoptosis Protein 2 in Gastric Carcinogenesis.
[So] Source:Gut Liver;11(1):79-86, 2017 Jan 15.
[Is] ISSN:2005-1212
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Background/Aims: To evaluate the expression of cellular inhibitor of apoptosis protein 2 ( ) during gastric carcinogenesis after (HP) infection and after HP eradication. Methods: We divided non-cancer patients into four groups according to the status of HP infection and atrophic gastritis (AG)/intestinal metaplasia (IM). We compared mRNA expression among these four groups and patients with HP-positive early gastric cancer (EGC) by using real-time polymerase chain reaction (PCR). We evaluated the expression of messenger RNA (mRNA)/protein by using real-time PCR/immunohistochemistry and the degree of apoptosis with a terminal deoxynucleotidyl transferasemediated nick end labeling assay before and 12 months after endoscopic submucosal dissection (ESD) in HP-positive EGC patients, regardless of whether they had undergone eradication therapy. Results: The expression of mRNA was significantly higher in the groups with HP(+), AG/IM(+), and HP-positive EGC than in the control, HP(+), and AG/ IM(-) groups (p<0.005). In the HP eradication group, the expression of mRNA/protein significantly decreased (p=0.006) and apoptosis increased at the 12-month follow-up after ESD. In the HP noneradication group, the aforementioned changes were not found during the same follow-up period. Conclusions: The expression of increased during gastric carcinogenesis after HP infection; HP eradication in the patients who had undergone ESD for EGC reversed overexpression of and suppressed cell apoptosis.
[Mh] Termos MeSH primário: Apoptose/genética
Carcinogênese/genética
Carcinoma/genética
Gastrite Atrófica/genética
Infecções por Helicobacter/genética
Proteínas Inibidoras de Apoptose/genética
RNA Mensageiro/metabolismo
Neoplasias Gástricas/genética
Ubiquitina-Proteína Ligases/genética
[Mh] Termos MeSH secundário: Amoxicilina/uso terapêutico
Antibacterianos/uso terapêutico
Proteína 3 com Repetições IAP de Baculovírus
Carcinoma/complicações
Carcinoma/patologia
Carcinoma/cirurgia
Claritromicina/uso terapêutico
Regulação para Baixo
Ressecção Endoscópica de Mucosa
Gastrite Atrófica/complicações
Gastrite Atrófica/metabolismo
Gastrite Atrófica/patologia
Infecções por Helicobacter/complicações
Infecções por Helicobacter/tratamento farmacológico
Infecções por Helicobacter/metabolismo
Helicobacter pylori
Seres Humanos
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Proteínas Inibidoras de Apoptose/metabolismo
Metaplasia
Estadiamento de Neoplasias
Omeprazol/uso terapêutico
Inibidores da Bomba de Prótons/uso terapêutico
Reação em Cadeia da Polimerase em Tempo Real
Estômago/patologia
Neoplasias Gástricas/complicações
Neoplasias Gástricas/patologia
Neoplasias Gástricas/cirurgia
Ubiquitina-Proteína Ligases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Inhibitor of Apoptosis Proteins); 0 (Proton Pump Inhibitors); 0 (RNA, Messenger); 804826J2HU (Amoxicillin); EC 2.3.2.27 (BIRC3 protein, human); EC 2.3.2.27 (Baculoviral IAP Repeat-Containing 3 Protein); EC 2.3.2.27 (Ubiquitin-Protein Ligases); H1250JIK0A (Clarithromycin); KG60484QX9 (Omeprazole)
[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:160611
[St] Status:MEDLINE
[do] DOI:10.5009/gnl15585


  8 / 263 MEDLINE  
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[PMID]:27074575
[Au] Autor:Gressot LV; Doucette T; Yang Y; Fuller GN; Manyam G; Rao A; Latha K; Rao G
[Ad] Endereço:Department of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
[Ti] Título:Analysis of the inhibitors of apoptosis identifies BIRC3 as a facilitator of malignant progression in glioma.
[So] Source:Oncotarget;8(8):12695-12704, 2017 Feb 21.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gliomas, the most common primary brain tumor in humans, include a spectrum of disease. High-grade gliomas (HGG), such as glioblastoma, may arise from low-grade gliomas (LGG) that have a more indolent course. The process of malignant transformation (MT) of LGG to HGG is poorly understood but likely involves the activation of signaling programs that suppress apoptosis. We previously showed that Survivin (BIRC5) plays a role in malignant progression of glioma. Here, we investigated the role of the remaining members of the Inhibitors of Apoptosis (IAP) family on promoting MT in glioma. Utilizing expression data from the cancer genome atlas (TCGA), we identified BIRC3 as a key facilitator of MT from LGG to HGG. TCGA HGGs with high expression of BIRC 3 demonstrated a survival disadvantage and expression levels of BIRC3 were also significantly higher in TCGA HGG compared to TCGA LGG cases. We validated our findings from TCGA by using matched human specimens to show that BIRC expression is increased in HGG compared to their precursor LGG lesions. Using a unique murine model of glioma, we show that overexpression of BIRC3 promotes higher grade glioma and significantly reduces tumor-free survival in mice.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/patologia
Transformação Celular Neoplásica/metabolismo
Glioma/patologia
Proteínas Inibidoras de Apoptose/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Proteína 3 com Repetições IAP de Baculovírus
Neoplasias Encefálicas/mortalidade
Transformação Celular Neoplásica/patologia
Progressão da Doença
Intervalo Livre de Doença
Glioma/mortalidade
Seres Humanos
Estimativa de Kaplan-Meier
Camundongos
Camundongos Transgênicos
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inhibitor of Apoptosis Proteins); EC 2.3.2.27 (BIRC3 protein, human); EC 2.3.2.27 (Baculoviral IAP Repeat-Containing 3 Protein); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160414
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.8657


  9 / 263 MEDLINE  
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[PMID]:27993143
[Au] Autor:Hatem J; Schrank-Hacker AM; Watt CD; Morrissette JJ; Rubin AI; Kim EJ; Nasta SD; Wasik MA; Bogusz AM
[Ad] Endereço:Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 7 E Gates Pavilion, 3400 Spruce Street, Philadelphia, 19104-4283, PA, USA.
[Ti] Título:Marginal zone lymphoma-derived interfollicular diffuse large B-cell lymphoma harboring 20q12 chromosomal deletion and missense mutation of BIRC3 gene: a case report.
[So] Source:Diagn Pathol;11(1):137, 2016 Dec 19.
[Is] ISSN:1746-1596
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Diffuse large B-cell lymphoma (DLBCL) typically leads to effacement of the nodal architecture by an infiltrate of malignant cells. Rarely (<1%), DLBCL can present with an interfollicular pattern (DLBCL-IF) preserving the lymphoid follicles. It has been postulated that DLBCL-IF is derived from marginal zone B cells and may represent a large-cell transformation of marginal zone lymphoma (MZL), however no direct evidence has been provided to date. Here we describe a rare case of a diagnostically challenging DLBCL-IF involving a lymph node in a patient with a prior history of lymphadenopathy for several years and MZL involving skin. CASE PRESENTATION: A 53-year old man presented to our Dermatology Clinic due to a 1-year history of generalized itching, fatigue of 2-3 month's duration, nausea and mid back rash that was biopsied. PET (positron emission tomography)/CT (computed tomography) was performed and revealed inguinal, pelvic, retroperitoneal, axillary, and cervical lymphadenopathy. The patient was referred to surgery for excisional biopsy of a right inguinal lymph node. Diagnostic H&E stained slides and ancillary studies were reviewed for the lymph node and skin specimens. B-cell clonality by PCR and sequencing studies were performed on both specimens. We demonstrate that this patient's MZL and DLBCL-IF are clonally related, strongly suggesting that transformation of MZL to DLBCL had occurred. Furthermore, we identified a novel deletion of the long arm of chromosome 20 (del(20q12)) and a missense mutation in BIRC3 (Baculoviral IAP repeat-containing protein 3) in this patient's DLBCL that are absent from his MZL, suggesting that these genetic alterations contributed to the large cell transformation. CONCLUSIONS: To our knowledge, this is the first report providing molecular evidence for a previously suspected link between MZL and DLBCL-IF. In addition, we describe for the first time del(20q12) and a missense mutation in BIRC3 in DLBCL. Our findings also raise awareness of DLBCL-IF and discuss the diagnostic pitfalls of this rare entity.
[Mh] Termos MeSH primário: Deleção Cromossômica
Cromossomos Humanos Par 20/genética
Proteínas Inibidoras de Apoptose/genética
Linfoma de Zona Marginal Tipo Células B/patologia
Linfoma Difuso de Grandes Células B/patologia
Mutação de Sentido Incorreto
Ubiquitina-Proteína Ligases/genética
[Mh] Termos MeSH secundário: Proteína 3 com Repetições IAP de Baculovírus
Biomarcadores Tumorais/análise
Citometria de Fluxo
Seres Humanos
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Linfoma de Zona Marginal Tipo Células B/genética
Linfoma Difuso de Grandes Células B/genética
Masculino
Meia-Idade
Reação em Cadeia da Polimerase
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Inhibitor of Apoptosis Proteins); EC 2.3.2.27 (BIRC3 protein, human); EC 2.3.2.27 (Baculoviral IAP Repeat-Containing 3 Protein); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[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:161221
[St] Status:MEDLINE


  10 / 263 MEDLINE  
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[PMID]:27534557
[Au] Autor:Akhtar N; Singh AK; Ahmed S
[Ad] Endereço:Department of Pharmaceutical Sciences, Washington State University College of Pharmacy, Spokane, WA 99210.
[Ti] Título:MicroRNA-17 Suppresses TNF-α Signaling by Interfering with TRAF2 and cIAP2 Association in Rheumatoid Arthritis Synovial Fibroblasts.
[So] Source:J Immunol;197(6):2219-28, 2016 Sep 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TNF-α is a major cytokine implicated in rheumatoid arthritis (RA), and its expression is regulated at the transcriptional and posttranscriptional levels. However, the impact of changes in microRNA expression on posttranslational processes involved in TNF-α signaling networks is not well defined in RA. In this study, we evaluated the effect of miR-17, a member of the miR-17-92 cluster, on the TNF-α signaling pathway in human RA synovial fibroblasts (SFs). We demonstrated that miR-17 expression was significantly low in RA serum, SFs, and synovial tissues, as well as in the serum and joints of adjuvant-induced arthritis rats. RNA-sequencing analysis showed modulation of 664 genes by pre-miR-17 in human RA SFs. Ingenuity pathway analysis of RNA-sequencing data identified the ubiquitin proteasome system in the TNF-α signaling pathway as a primary target of miR-17. Western blot analysis confirmed the reduction in TRAF2, cIAP1, cIAP2, USP2, and PSMD13 expression by miR-17 in TNF-α-stimulated RA SFs. Immunoprecipitation assays showed that miR-17 restoration increased the K48-linked polyubiquitination of TRAF2, cIAP1, and cIAP2 in TNF-α-stimulated RA SFs. Thus, destabilization of TRAF2 by miR-17 reduced the ability of TRAF2 to associate with cIAP2, resulting in the downregulation of TNF-α-induced NF-κBp65, c-Jun, and STAT3 nuclear translocation and the production of IL-6, IL-8, MMP-1, and MMP-13 in human RA SFs. In conclusion, this study provides evidence for the role of miR-17 as a negative regulator of TNF-α signaling by modulating the protein ubiquitin processes in RA SFs.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Proteínas Inibidoras de Apoptose/fisiologia
MicroRNAs/fisiologia
Membrana Sinovial/imunologia
Fator 2 Associado a Receptor de TNF/fisiologia
Fator de Necrose Tumoral alfa/farmacologia
Ubiquitina-Proteína Ligases/fisiologia
[Mh] Termos MeSH secundário: Artrite Reumatoide/etiologia
Proteína 3 com Repetições IAP de Baculovírus
Células Cultivadas
Citocinas/biossíntese
Fibroblastos/imunologia
Seres Humanos
Sistema de Sinalização das MAP Quinases/fisiologia
Metaloproteinase 1 da Matriz/biossíntese
NF-kappa B/fisiologia
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Ubiquitina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inhibitor of Apoptosis Proteins); 0 (MIRN17 microRNA, human); 0 (MicroRNAs); 0 (NF-kappa B); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (TNF Receptor-Associated Factor 2); 0 (Tumor Necrosis Factor-alpha); 0 (Ubiquitin); EC 2.3.2.27 (BIRC3 protein, human); EC 2.3.2.27 (Baculoviral IAP Repeat-Containing 3 Protein); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.4.24.7 (Matrix Metalloproteinase 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160819
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600360



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