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  1 / 2091 MEDLINE  
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[PMID]:29235796
[Au] Autor:Minchenko OH; Tsymbal DO; Minchenko DO; Ratushna OO
[Ti] Título:The role of the TNF receptors and apoptosis inducing ligands in tumor growth.
[So] Source:Ukr Biochem J;88(5):18-37, 2016 Seo-Oct.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor (TNF) superfamily receptors and TNF apoptosis inducing ligands play an important role in the realization of TNF function and control tumor growth. The TNF-related pathways are controlled by endoplasmic reticulum stress signaling, which has a crucial role in the control of cell proliferation and tumor growth. Furthermore, the inhibition of IRE1 (inositol requiring enzyme-1), which is a central mediator of endoplasmic reticulum stress sand mainly responsible for cell proliferation and apoptosis, leads to suppression of tumor growth through specific changes in the expression of genes encoding transcription factors, tumor suppressors, angiogenesis and apoptosis related proteins, including TNF superfamily receptors and TNF apoptosis inducing ligands. Therefore, changes in the expression level of TNF-related genes encoding TNF superfamily receptors and apoptosis inducing ligands possibly reflect metabolic reprogramming of cancer cells upon inhibition of IRE1-mediated endoplasmic reticulum stress signaling and correlate with suppression of glioma cell proliferation.
[Mh] Termos MeSH primário: Apoptose/genética
Neoplasias Encefálicas/genética
Endorribonucleases/genética
Regulação Neoplásica da Expressão Gênica
Glioma/genética
Proteínas Serina-Treonina Quinases/genética
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética
[Mh] Termos MeSH secundário: Proteínas Reguladoras de Apoptose/genética
Proteínas Reguladoras de Apoptose/metabolismo
Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/patologia
Linhagem Celular Tumoral
Proliferação Celular
Estresse do Retículo Endoplasmático/genética
Endorribonucleases/deficiência
Glioma/metabolismo
Glioma/patologia
Seres Humanos
Proteínas Serina-Treonina Quinases/deficiência
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Transdução de Sinais
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Proteínas Supressoras de Tumor/genética
Proteínas Supressoras de Tumor/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (Transcription Factors); 0 (Tumor Suppressor Proteins); EC 2.7.11.1 (ERN1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.1.- (Endoribonucleases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.05.018


  2 / 2091 MEDLINE  
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[PMID]:29187434
[Au] Autor:Manouchehri JM; Kalafatis M
[Ad] Endereço:Department of Chemistry, Science and Research Center, Cleveland State University, Cleveland, OH, U.S.A.
[Ti] Título:Sensitization of rhTRAIL-resistant Triple-negative Breast Carcinoma Through Silibinin Co-Treatment.
[So] Source:Anticancer Res;37(12):6593-6599, 2017 12.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Triple-negative breast cancer (TNBC) is the most fatal form of breast cancer due to the shortcomings of therapies. However, recombinant human tumor necrosis factor-related apoptosis-inducing ligand (rhTRAIL) is a promising anticancer therapeutic that possesses the capability to promote the induction of apoptosis in cancer cells, but some TNBCs are resistant to rhTRAIL's pro-apoptotic effects. Therefore, a combinatorial treatment approach with silibinin and rhTRAIL was considered in order to sensitize rhTRAIL-resistant TNBCs. MATERIALS AND METHODS: The co-treatment of rhTRAIL and silibinin's impact on apoptosis induction in rhTRAIL-resistant TNBC BT-20 and HCC1937 cells was inspected via application of Annexin V/PI assays and western blot analysis. RESULTS: Silibinin possessed the ability to sensitize the examined rhTRAIL-resistant TNBC cells to rhTRAIL-induced apoptosis through the up-regulation of death receptors 4 and 5 and the down-regulation of survivin transcriptionally. CONCLUSION: Silibinin is a good sensitizing agent for rhTRAIL-resistant TNBCs.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Silimarina/farmacologia
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
[Mh] Termos MeSH secundário: Apoptose/genética
Western Blotting
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos/genética
Sinergismo Farmacológico
Feminino
Citometria de Fluxo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Proteínas Inibidoras de Apoptose/genética
Proteínas Inibidoras de Apoptose/metabolismo
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Proteínas Recombinantes/farmacologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Ligante Indutor de Apoptose Relacionado a TNF/genética
Neoplasias de Mama Triplo Negativas/genética
Neoplasias de Mama Triplo Negativas/metabolismo
Neoplasias de Mama Triplo Negativas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BIRC5 protein, human); 0 (Inhibitor of Apoptosis Proteins); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (Recombinant Proteins); 0 (Silymarin); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFRSF10B protein, human); 4RKY41TBTF (silybin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE


  3 / 2091 MEDLINE  
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[PMID]:28444885
[Au] Autor:Yin J; Ni B; Liao WG; Gao YQ
[Ad] Endereço:Department of Pathophysiology and High Altitude Pathology/Key Laboratory of High Altitude Environment Medicine (Third Military Medical University), Ministry of Education/Key Laboratory of High Altitude Medicine, College of High Altitude Military Medicine, Third Military Medical University, Chongqing
[Ti] Título:Hypoxia-induced apoptosis of mouse spermatocytes is mediated by HIF-1α through a death receptor pathway and a mitochondrial pathway.
[So] Source:J Cell Physiol;233(2):1146-1155, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypoxia in vivo induces oligozoospermia, azoospermia, and degeneration of the germinal epithelium, but the underlying molecular mechanism of this induction is not fully clarified. The aim of this study was to investigate the role of the death receptor pathway and the mitochondrial pathway in hypoxia-induced apoptosis of mouse GC-2spd (GC-2) cells and the relationship between HIF-1α and apoptosis of GC-2 cells induced by hypoxia. GC-2 cells were subjected to 1% oxygen for 48 hr. Apoptosis was detected by flow cytometry, TUNEL staining, LDH, caspase-3/8/9 in the absence and presence of HIF-1α siRNA. The protein levels of apoptosis-related markers were determined by Western blot in the presence and absence of HIF-1α siRNA. Mitochondrial transmembrane potential change was observed by in situ JC-1 staining. Cell viability was assessed upon treatment of caspase-8 and 9 inhibitors. The results indicated that hypoxia at 1% oxygen for 48 hr induced apoptosis of GC-2 cells. A prolonged exposure of GC-2 cells to hypoxic conditions caused downregulation of c-FLIP, D R and Bcl-2 and upregulation of DR , TRAIL, Fas, p53, and Bax, with an overproduction of caspase-3/8/9. Moreover, hypoxia at this level had an effect on mitochondrial depolarization. In addition, specific inhibitors of caspase-8/9 partially suppressed hypoxia-induced GC-2 cell apoptosis, and the anti-apoptotic effects of the caspase inhibitors were additive. Of note, HIF-1α knockdown attenuated hypoxia and induced apoptosis of GC-2 cells. In conclusion, our data suggest that the death receptor pathway and mitochondrial pathway, which are likely mediated by HIF-1α, contribute to hypoxia-induced GC-2 cell apoptosis.
[Mh] Termos MeSH primário: Apoptose
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Mitocôndrias/metabolismo
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Transdução de Sinais
Espermatócitos/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Proteínas Reguladoras de Apoptose/genética
Proteínas Reguladoras de Apoptose/metabolismo
Inibidores de Caspase/farmacologia
Hipóxia Celular
Linhagem Celular
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Masculino
Potencial da Membrana Mitocondrial
Camundongos
Mitocôndrias/patologia
Interferência de RNA
Transdução de Sinais/efeitos dos fármacos
Espermatócitos/efeitos dos fármacos
Espermatócitos/patologia
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (Caspase Inhibitors); 0 (Hif1a protein, mouse); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (Tnfrsf10b protein, mouse)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25974


  4 / 2091 MEDLINE  
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[PMID]:29017180
[Au] Autor:Cassier PA; Castets M; Belhabri A; Vey N
[Ad] Endereço:Department of Medical Oncology, Centre Léon Bérard, 69008 Lyon, France.
[Ti] Título:Targeting apoptosis in acute myeloid leukaemia.
[So] Source:Br J Cancer;117(8):1089-1098, 2017 Oct 10.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Acute myeloid leukaemia (AML) is a molecularly and clinically heterogeneous disease, and its incidence is increasing as the populations in Western countries age. Despite major advances in understanding the genetic landscape of AML and its impact on the biology of the disease, standard therapy has not changed significantly in the last three decades. Allogeneic haematopoietic stem cell transplantation remains the best chance for cure, but can only be offered to a minority of younger fit patients. Molecularly targeted drugs aiming at restoring apoptosis in leukaemic cells have shown encouraging activity in early clinical trials and some of these drugs are currently being evaluated in randomised controlled trials. In this review, we discuss the current development of drugs designed to trigger cell death in AML.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Apoptose
Proteínas Inibidoras de Apoptose/antagonistas & inibidores
Leucemia Mieloide Aguda/terapia
Proteínas Proto-Oncogênicas c-bcl-2/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-mdm2/antagonistas & inibidores
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/antagonistas & inibidores
[Mh] Termos MeSH secundário: Transplante de Células-Tronco Hematopoéticas
Seres Humanos
Terapia de Alvo Molecular
Receptores do Ligante Indutor de Apoptose Relacionado a TNF
Proteína Supressora de Tumor p53
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Inhibitor of Apoptosis Proteins); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (Tumor Suppressor Protein p53); 0 (X-Linked Inhibitor of Apoptosis Protein); EC 2.3.2.27 (Proto-Oncogene Proteins c-mdm2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.281


  5 / 2091 MEDLINE  
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[PMID]:28834692
[Au] Autor:Vunnam N; Lo CH; Grant BD; Thomas DD; Sachs JN
[Ad] Endereço:Department of Biomedical Engineering, University of Minnesota, Minneapolis, MN 55455, United States.
[Ti] Título:Soluble Extracellular Domain of Death Receptor 5 Inhibits TRAIL-Induced Apoptosis by Disrupting Receptor-Receptor Interactions.
[So] Source:J Mol Biol;429(19):2943-2953, 2017 Sep 15.
[Is] ISSN:1089-8638
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dysregulation of tumor necrosis factor (TNF) receptor signaling is a key feature of various inflammatory disorders. Current treatments for TNF-related diseases function either by sequestering ligand or blocking ligand-receptor interactions, which can cause dangerous side effects by inhibiting the receptors that are not involved in the disease condition. Thus, alternate strategies that target receptor-receptor interactions are needed. We hypothesized that the soluble extracellular domain (ECD) of long isoform of death receptor 5 (DR5) could block endogenous receptor assembly, mimicking the biological effect of decoy receptors that lack the death domain to trigger apoptosis. Using live-cell fluorescence resonance energy transfer studies, we demonstrated that soluble ECD disrupts endogenous DR5-DR5 interactions. Cell viability assays were used to demonstrate the complete inhibition of TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by the ECD, although TRAIL is still able to bind to the receptor. Importantly, we used mutagenesis to prove that the inhibition of TRAIL-induced apoptosis by the ECD predominantly comes from the disruption of DR5 oligomerization and not ligand sequestration. Inhibition of death receptor activation should have important therapeutic applications in diseases such as nonalcoholic fatty liver disease. More generally, this approach should be generalized to enable the inhibition of other TNF receptor signaling mechanisms that are associated in a wide range of clinical conditions.
[Mh] Termos MeSH primário: Apoptose
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Sobrevivência Celular
Análise Mutacional de DNA
Transferência Ressonante de Energia de Fluorescência
Seres Humanos
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética
Transdução de Sinais
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE


  6 / 2091 MEDLINE  
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[PMID]:28571773
[Au] Autor:Hwang JS; Lee YY; Lee DH; Kwon KH
[Ad] Endereço:Division of Cosmetic Arts, Department of Culture Service, Graduate School of Culture and Arts, Dongguk University, Republic of Korea.
[Ti] Título:DATS sensitizes glioma cells to TRAIL-mediated apoptosis by up-regulation of death receptor 5 via ROS.
[So] Source:Food Chem Toxicol;106(Pt A):514-521, 2017 Aug.
[Is] ISSN:1873-6351
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor-related apoptosis-induced ligand (TRAIL) is a promising anticancer reagent for antitumor therapy. However, many cancer cells, including malignant glioma cells, tend to be resistant to TRAIL, due to repeat treat to cancer cells, highlighting the need for strategies to overcome TRAIL resistance. Here we present that in combination with diallyl trisulfide (DATS), exposure to TRAIL induced apoptosis in TRAIL-resistant glioma cells. Surprisingly, we found that subtoxic concentrations of DATS significantly potentiated TRAIL-induced cytotoxicity and apoptosis in glioma cells. DATS dramatically upregulated DR5 receptor expression but had no effects on DR4 receptor. In addition, DATS enhances TRAIL-induced apoptosis through the downregulation of anti-apoptotic protein (Mcl-1) and the upregulation of DR5 receptors through actions on the ROS- induced-p53.
[Mh] Termos MeSH primário: Compostos Alílicos/farmacologia
Apoptose/efeitos dos fármacos
Glioma/genética
Espécies Reativas de Oxigênio/metabolismo
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Sulfetos/farmacologia
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Glioma/tratamento farmacológico
Glioma/metabolismo
Glioma/fisiopatologia
Seres Humanos
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética
Ligante Indutor de Apoptose Relacionado a TNF/genética
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allyl Compounds); 0 (Reactive Oxygen Species); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (Sulfides); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (Tumor Necrosis Factor-alpha); 0ZO1U5A3XX (diallyl trisulfide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE


  7 / 2091 MEDLINE  
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[PMID]:28536452
[Au] Autor:von Karstedt S; Montinaro A; Walczak H
[Ad] Endereço:Centre for Cell Death, Cancer and Inflammation, UCL Cancer Institute, University College London, 72 Huntley Street, London WC1E 6DD, UK.
[Ti] Título:Exploring the TRAILs less travelled: TRAIL in cancer biology and therapy.
[So] Source:Nat Rev Cancer;17(6):352-366, 2017 May 24.
[Is] ISSN:1474-1768
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The discovery that the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis of cancer cells without causing toxicity in mice has led to the in-depth study of pro-apoptotic TRAIL receptor (TRAIL-R) signalling and the development of biotherapeutic drug candidates that activate TRAIL-Rs. The outcome of clinical trials with these TRAIL-R agonists has, however, been disappointing so far. Recent evidence indicates that many cancers, in addition to being TRAIL resistant, use the endogenous TRAIL-TRAIL-R system to their own advantage. However, novel insight on two fronts - how resistance of cancer cells to TRAIL-based pro-apoptotic therapies might be overcome, and how the pro-tumorigenic effects of endogenous TRAIL might be countered - gives reasonable hope that the TRAIL system can be harnessed to treat cancer. In this Review we assess the status quo of our understanding of the biology of the TRAIL-TRAIL-R system - as well as the gaps therein - and discuss the opportunities and challenges in effectively targeting this pathway.
[Mh] Termos MeSH primário: Neoplasias/etiologia
Neoplasias/terapia
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/fisiologia
Ligante Indutor de Apoptose Relacionado a TNF/fisiologia
[Mh] Termos MeSH secundário: Seres Humanos
Neoplasias/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (TNF-Related Apoptosis-Inducing Ligand)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170826
[Lr] Data última revisão:
170826
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170525
[St] Status:MEDLINE
[do] DOI:10.1038/nrc.2017.28


  8 / 2091 MEDLINE  
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[PMID]:28506821
[Au] Autor:Shim J; Huang A; Miller AS
[Ad] Endereço:Biological Technologies-Analytical Development and Quality Control, Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080, USA. Electronic address: shim.jeongsup@gene.com.
[Ti] Título:Development of a bioassay as a measure of drozitumab-mediated apoptosis induced by soluble Fc gamma receptors.
[So] Source:J Immunol Methods;448:26-33, 2017 Sep.
[Is] ISSN:1872-7905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Drozitumab is an agonistic therapeutic monoclonal antibody (mAb) against the pro-apoptotic death receptor 5 (DR5). In vitro cell killing assays using drozitumab have traditionally required cross-linking with anti-Fc antibody to amplify the pro-apoptotic signal, although drozitumab shows activity in in vivo tumor models without artificial cross-linking. Recently it has been shown that FcγR expressing cells play an important role in the activity of drozitumab by mediating cross-linking in vivo (Wilson et al., 2011). To provide a more biologically relevant alternative to cross-linking with anti-Fc antibody in in vitro bioassays, methods for cross-linking with soluble FcγR extracellular domain (ECD) were developed in this work. FcγR cross-linking methods developed in this work were assessed in solution, bead-bound, and plate-bound assay formats, as well as a cell-based assay format. The assays showed reproducible drozitumab dose-response curves in the concentration range of 5-20,000ng/mL and had acceptable precision and accuracy. The assays are also able to detect degradative changes in drozitumab samples subjected to thermal stress. The data suggest that FcγR cross-linking of drozitumab is a viable alternative to anti-Fc cross-linking of drozitumab to measure effector mediated apoptosis of drozitumab in vitro.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Imunoensaio/métodos
Receptores de IgG/metabolismo
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/antagonistas & inibidores
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/química
Anticorpos Monoclonais/metabolismo
Antineoplásicos/química
Antineoplásicos/metabolismo
Técnicas de Cocultura
Relação Dose-Resposta a Droga
Estabilidade de Medicamentos
Células HEK293
Temperatura Alta
Seres Humanos
Células Jurkat
Microscopia
Ligação Proteica
Desnaturação Proteica
Domínios e Motivos de Interação entre Proteínas
Estabilidade Proteica
Receptores de IgG/química
Receptores de IgG/imunologia
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/imunologia
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Reprodutibilidade dos Testes
Transdução de Sinais/efeitos dos fármacos
Ressonância de Plasmônio de Superfície
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 0 (Receptors, IgG); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (TNFRSF10B protein, human); SQ67484MA7 (drozitumab)
[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:170517
[St] Status:MEDLINE


  9 / 2091 MEDLINE  
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[PMID]:28476883
[Au] Autor:Yang SZ; Xu F; Zhou T; Zhao X; McDonald JM; Chen Y
[Ad] Endereço:From the Departments of Pathology.
[Ti] Título:The long non-coding RNA HOTAIR enhances pancreatic cancer resistance to TNF-related apoptosis-inducing ligand.
[So] Source:J Biol Chem;292(25):10390-10397, 2017 Jun 23.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pancreatic cancer is a malignant neoplasm with a high mortality rate. Therapeutic agents that activate TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis have shown promising efficacy, but many pancreatic cancers are resistant to TRAIL therapy. Epigenetic regulation plays important roles in tumor pathogenesis and resistance, and a recent study indicated that the long non-coding RNA HOX transcript antisense RNA (HOTAIR) is overexpressed in pancreatic cancer. However, the role of HOTAIR in pancreatic cancer resistance to anticancer agents is unknown. The present study determined the role of HOTAIR in pancreatic cancer TRAIL resistance and investigated the underlying molecular mechanisms. We observed that TRAIL-resistant pancreatic cancer cells had higher levels of HOTAIR expression, whereas TRAIL-sensitive pancreatic cancer cells had lower HOTAIR levels. Overexpressing HOTAIR in TRAIL-sensitive cells attenuated TRAIL-induced apoptosis, and shRNA-mediated HOTAIR knockdown in TRAIL-resistant PANC-1 cells sensitized them to TRAIL-induced apoptosis. These results support a causative effect of HOTAIR on TRAIL sensitivity. Mechanistically, we found that increased HOTAIR expression inhibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR knockdown increased DR5 expression. We further demonstrated that HOTAIR regulates DR5 expression via the epigenetic regulator enhancer of zeste homolog 2 (EZH2) and that EZH2 controls histone H3 lysine 27 trimethylation on the gene. Taken together, these results demonstrate that high HOTAIR levels increase the resistance of pancreatic cancer cells to TRAIL-induced apoptosis via epigenetic regulation of DR5 expression. Our study therefore supports the notion that targeting HOTAIR function may represent a strategy to overcome TRAIL resistance in pancreatic cancer.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Neoplasias Pancreáticas/metabolismo
RNA Longo não Codificante/biossíntese
RNA Neoplásico/biossíntese
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proteína Potenciadora do Homólogo 2 de Zeste/biossíntese
Proteína Potenciadora do Homólogo 2 de Zeste/genética
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Histonas/genética
Histonas/metabolismo
Seres Humanos
Metilação/efeitos dos fármacos
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/patologia
RNA Longo não Codificante/genética
RNA Neoplásico/genética
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/biossíntese
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HOTAIR long untranslated RNA, human); 0 (Histones); 0 (Neoplasm Proteins); 0 (RNA, Long Noncoding); 0 (RNA, Neoplasm); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFRSF10B protein, human); 0 (TNFSF10 protein, human); EC 2.1.1.43 (EZH2 protein, human); EC 2.1.1.43 (Enhancer of Zeste Homolog 2 Protein)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.786830


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[PMID]:28393201
[Au] Autor:Li X; Yang B; Wang L; Chen L; Luo X; Liu L
[Ad] Endereço:Department of Hematology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
[Ti] Título:SPAG6 regulates cell apoptosis through the TRAIL signal pathway in myelodysplastic syndromes.
[So] Source:Oncol Rep;37(5):2839-2846, 2017 May.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Myelodysplastic syndromes (MDSs) are a group of malignant clone hematopoietic stem-cell diseases, and the evolution and progression of MDS depend on the abnormal apoptosis of bone marrow cells. Our previous studies have indicated that sperm-associated antigen 6 (SPAG6), located in the uniparental disomy regions of myeloid cells, is overexpressed in patients with MDS as compared to controls, and SPAG6 can inhibit apoptosis of SKM-1. However, the concrete mechanism is still unclear. In the present study, it was found that the TNF-related apoptosis-inducing ligand (TRAIL)signal pathway was activated when the expression of SPAG6 was inhibited by SPAG6-shRNA lentivirus in SKM-1 cells. Additionally, the results of flow cytometry, Cell Counting Kit-8 assay and western blot analysis implied that the TRAIL signal pathway could be inhibited by a high expression of SPAG6. However, SPAG6 cannot influence the expression of TRAIL death receptors, except for FADD. Additionally the interaction between FADD and TRAIL death receptors also increased in SKM-1 cells infected with SPAG6-shRNA lentivirus. Thus, our study demonstrates that SPAG6 may regulate apoptosis in SKM-1 through the TRAIL signal pathway, indicating that SPAG6 could be a potential therapeutic target.
[Mh] Termos MeSH primário: Proteína de Domínio de Morte Associada a Fas/metabolismo
Proteínas dos Microtúbulos/genética
Síndromes Mielodisplásicas/genética
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
[Mh] Termos MeSH secundário: Apoptose
Linhagem Celular Tumoral
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Células K562
Proteínas dos Microtúbulos/metabolismo
Síndromes Mielodisplásicas/metabolismo
RNA Interferente Pequeno/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FADD protein, human); 0 (Fas-Associated Death Domain Protein); 0 (Microtubule Proteins); 0 (RNA, Small Interfering); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (SPAG6 protein, human); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFSF10 protein, human)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.3892/or.2017.5540



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