Base de dados : MEDLINE
Pesquisa : D12.776.543.750.705.852.760.949.500 [Categoria DeCS]
Referências encontradas : 160 [refinar]
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[PMID]:28420351
[Au] Autor:Labovsky V; Martinez LM; Davies KM; de Luján Calcagno M; García-Rivello H; Wernicke A; Feldman L; Matas A; Giorello MB; Borzone FR; Choi H; Howard SC; Chasseing NA
[Ad] Endereço:Instituto de Biología y Medicina Experimental, Laboratorio de Inmunohematología (IBYME) - Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Vuelta de Obligado 2490, CP 1428, Ciudad Autónoma de Buenos Aires, Argentina. 16vivian@gmail.com.
[Ti] Título:Prognostic significance of TRAIL-R3 and CCR-2 expression in tumor epithelial cells of patients with early breast cancer.
[So] Source:BMC Cancer;17(1):280, 2017 04 18.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Tumor epithelial cells (TEpCs) and spindle-shaped stromal cells, not associated with the vasculature, of patients with early breast cancer express osteoprotegerin (OPG), tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), receptor activator of nuclear factor kappa B ligand, stromal cell derived factor-1, interleukin-6, macrophage colony stimulating factor, chemokine (C-C motif) ligand-2 (CCL-2) and their receptors at significantly higher levels compared with non-neoplastic breast tissues. We evaluated the clinicopathological significance of these ligands and receptors in TEpC and spindle-shaped stromal cells, not associated with the vasculature, to determine their impact on prognosis of patients with early-stage breast cancer. METHODS: We conducted immunohistochemical analyses of protein expression in primary tumors of patients with early breast cancer and analyzed their association with standard prognostic parameters and clinical outcomes, including local relapse, metastatic recurrence, disease-free survival (DFS), metastasis-free survival (MFS), and overall survival (OS). RESULTS: Elevated levels of TRAIL-R3 and chemokine (C-C motif) receptor 2 (CCR-2) in TEpCs and OPG and CCL-2 in stromal cells were significantly associated with a higher risk of metastasis (p = 0.032, p = 0.003, p = 0.038, and p = 0.049; respectively). Moreover, high expression of TRAIL-R3 and CCR-2 in TEpCs was associated with shorter DFS, MFS, and OS. High TRAIL-R3 expression in TEpCs was an independent prognostic factor for DFS and OS, and high CCR-2 expression in these cells was an independent prognostic factor for MFS. CONCLUSIONS: High levels of TRAIL-R3 and CCR-2 expression in TEpCs identified patients with early breast cancer with poor outcomes.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Neoplasias da Mama/patologia
Células Epiteliais/metabolismo
Receptores CCR2/biossíntese
Membro 10c de Receptores do Fator de Necrose Tumoral/biossíntese
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Neoplasias da Mama/mortalidade
Células Epiteliais/patologia
Feminino
Proteínas Ligadas por GPI/análise
Proteínas Ligadas por GPI/biossíntese
Seres Humanos
Imuno-Histoquímica
Meia-Idade
Prognóstico
Receptores CCR2/análise
Membro 10c de Receptores do Fator de Necrose Tumoral/análise
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CCR2 protein, human); 0 (GPI-Linked Proteins); 0 (Receptors, CCR2); 0 (Receptors, Tumor Necrosis Factor, Member 10c); 0 (TNFRSF10C protein, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-017-3259-8


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[PMID]:28189700
[Au] Autor:Fardo DW; Katsumata Y; Kauwe JS; Deming Y; Harari O; Cruchaga C; Nelson PT; Alzheimer's Disease Neuroimaging Initiative
[Ad] Endereço:Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA; Department of Biostatistics, College of Public Health, University of Kentucky, Lexington, KY, USA. Electronic address: david.fardo@uky.edu.
[Ti] Título:CSF protein changes associated with hippocampal sclerosis risk gene variants highlight impact of GRN/PGRN.
[So] Source:Exp Gerontol;90:83-89, 2017 Apr.
[Is] ISSN:1873-6815
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Hippocampal sclerosis of aging (HS-Aging) is a common cause of dementia in older adults. We tested the variability in cerebrospinal fluid (CSF) proteins associated with previously identified HS-Aging risk single nucleotide polymorphisms (SNPs). METHODS: Alzheimer's Disease Neuroimaging Initiative cohort (ADNI; n=237) data, combining both multiplexed proteomics CSF and genotype data, were used to assess the association between CSF analytes and risk SNPs in four genes (SNPs): GRN (rs5848), TMEM106B (rs1990622), ABCC9 (rs704180), and KCNMB2 (rs9637454). For controls, non-HS-Aging SNPs in APOE (rs429358/rs7412) and MAPT (rs8070723) were also analyzed against Aß1-42 and total tau CSF analytes. RESULTS: The GRN risk SNP (rs5848) status correlated with variation in CSF proteins, with the risk allele (T) associated with increased levels of AXL Receptor Tyrosine Kinase (AXL), TNF-Related Apoptosis-Inducing Ligand Receptor 3 (TRAIL-R3), Vascular Cell Adhesion Molecule-1 (VCAM-1) and clusterin (CLU) (all p<0.05 after Bonferroni correction). The TRAIL-R3 correlation was significant in meta-analysis with an additional dataset (p=5.05×10 ). Further, the rs5848 SNP status was associated with increased CSF tau protein - a marker of neurodegeneration (p=0.015). These data are remarkable since this GRN SNP has been found to be a risk factor for multiple types of dementia-related brain pathologies.
[Mh] Termos MeSH primário: Envelhecimento/líquido cefalorraquidiano
Biomarcadores/líquido cefalorraquidiano
Demência/genética
Hipocampo/patologia
Peptídeos e Proteínas de Sinalização Intercelular/genética
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Peptídeos beta-Amiloides/líquido cefalorraquidiano
Clusterina/líquido cefalorraquidiano
Bases de Dados Factuais
Demência/líquido cefalorraquidiano
Feminino
Proteínas Ligadas por GPI/líquido cefalorraquidiano
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Masculino
Polimorfismo de Nucleotídeo Único
Membro 10c de Receptores do Fator de Necrose Tumoral/líquido cefalorraquidiano
Análise de Regressão
Fatores de Risco
Esclerose
Molécula 1 de Adesão de Célula Vascular/líquido cefalorraquidiano
Proteínas tau/líquido cefalorraquidiano
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Biomarkers); 0 (Clusterin); 0 (GPI-Linked Proteins); 0 (GRN protein, human); 0 (Intercellular Signaling Peptides and Proteins); 0 (Receptors, Tumor Necrosis Factor, Member 10c); 0 (TNFRSF10C protein, human); 0 (Vascular Cell Adhesion Molecule-1); 0 (tau Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170213
[St] Status:MEDLINE


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[PMID]:28119237
[Au] Autor:Xu Y; Li J; Li QJ; Feng YL; Pan F
[Ad] Endereço:Huai'an First People's Hospital, Nanjing Medical University, No. 6 Beijing West Road, Huaiyin District, Huai'an, Jiangsu 223300, China.
[Ti] Título:Betulinic acid promotes TRAIL function on liver cancer progression inhibition through p53/Caspase-3 signaling activation.
[So] Source:Biomed Pharmacother;88:349-358, 2017 Apr.
[Is] ISSN:1950-6007
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Betulinic acid (BA), isolated from the tree bark, is a pentacyclic triterpenoid, showing inhibitory role in cancer cells. However, the effects of BA treatment on liver cancer have little to be known. Thus, the study is conducted to explore the in vitro and in vivo role of BA in liver cancer. And the interactions between BA and tumor necrosis factor-related apoptosis-inducing ligand of APO2, also known as TRAIL, were investigated in liver cancer cells. A synergistic effect of BA and APO2 combination on apoptosis induction in liver cancer cells was observed. The cancer cells were insensitive to APO2 single therapy. However, liver cancer cells receiving BA were sensitive to APO2-triggered apoptotic response by enhancing Caspases cleavage, due to elevation of decoy receptor 1 and 2 (DcR1 and DcR2) dependent on p53. Bcl-2 family members of Bcl-2 and Mcl-1, belonging to anti-apoptosis, were decreased, whereas Bad and Bak, as pro-apoptotic members, were increased for BA and APO2 combined treatment. Additionally, the mouse xenograft model suggested that BA and APO2 in combination markedly inhibited liver cancer growth in comparison to BA or APO2 monotherapy without toxicity. The present study revealed a dramatically therapeutic strategy for promoting APO2-induced anti-cancer effects on liver cancer cells via BA combination.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Caspase 3/efeitos dos fármacos
Neoplasias Hepáticas/tratamento farmacológico
Transdução de Sinais/efeitos dos fármacos
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Triterpenos/farmacologia
Proteína Supressora de Tumor p53/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Proteínas Reguladoras de Apoptose/metabolismo
Linhagem Celular Tumoral
Proteínas Ligadas por GPI/metabolismo
Seres Humanos
Neoplasias Hepáticas/patologia
Camundongos
Camundongos Nus
Membro 10c de Receptores do Fator de Necrose Tumoral/metabolismo
Ligante Indutor de Apoptose Relacionado a TNF/efeitos dos fármacos
Receptores Chamariz do Fator de Necrose Tumoral/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Ensaio Tumoral de Célula-Tronco
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Apoptosis Regulatory Proteins); 0 (GPI-Linked Proteins); 0 (Receptors, Tumor Necrosis Factor, Member 10c); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFRSF10C protein, human); 0 (TNFRSF10D protein, human); 0 (TNFSF10 protein, human); 0 (Triterpenes); 0 (Tumor Necrosis Factor Decoy Receptors); 0 (Tumor Necrosis Factor-alpha); 0 (Tumor Suppressor Protein p53); 4G6A18707N (betulinic acid); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE


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[PMID]:26542757
[Au] Autor:Narayan G; Xie D; Ishdorj G; Scotto L; Mansukhani M; Pothuri B; Wright JD; Kaufmann AM; Schneider A; Arias-Pulido H; Murty VV
[Ad] Endereço:Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY.
[Ti] Título:Epigenetic inactivation of TRAIL decoy receptors at 8p12-21.3 commonly deleted region confers sensitivity to Apo2L/trail-Cisplatin combination therapy in cervical cancer.
[So] Source:Genes Chromosomes Cancer;55(2):177-89, 2016 Feb.
[Is] ISSN:1098-2264
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Multiple chromosomal regions are affected by deletions in cervical cancer (CC) genomes, but their consequence and target gene involvement remains unknown. Our single nucleotide polymorphism (SNP) array identified 8p copy number losses localized to an 8.4 Mb minimal deleted region (MDR) in 36% of CC. The 8p MDR was associated with tumor size, treatment outcome, and with multiple HPV infections. Genetic, epigenetic, and expression analyses of candidate genes at MDR identified promoter hypermethylation and/or inactivation of decoy receptors TNFRSF10C and TNFRSF10D in the majority of CC patients. TNFRSF10C methylation was also detected in precancerous lesions suggesting that this change is an early event in cervical tumorigenesis. We further demonstrate here that CC cell lines exhibiting downregulated expression of TNFRSF10C and/or TNFRSF10D effectively respond to TRAIL-induced apoptosis and this affect was synergistic in combination with DNA damaging chemotherapeutic drugs. We show that the CC cell lines harboring epigenetic inactivation of TRAIL decoy receptors effectively activate downstream caspases suggesting a critical role of inactivation of these genes in efficient execution of extrinsic apoptotic pathway and therapy response. Therefore, these findings shed new light on the role of genetic/epigenetic defects in TRAIL decoy receptor genes in the pathogenesis of CC and provide an opportunity to explore strategies to test decoy receptor gene inactivation as a biomarker of response to Apo2L/TRAIL-combination therapy.
[Mh] Termos MeSH primário: Cisplatino/farmacologia
Metilação de DNA
Membro 10c de Receptores do Fator de Necrose Tumoral/genética
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
Receptores Chamariz do Fator de Necrose Tumoral/genética
Neoplasias do Colo do Útero/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Protocolos de Quimioterapia Combinada Antineoplásica
Sequência de Bases
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Cromossomos Humanos Par 8/genética
Cisplatino/uso terapêutico
Epigênese Genética
Feminino
Proteínas Ligadas por GPI/genética
Células HeLa
Seres Humanos
Meia-Idade
Polimorfismo de Nucleotídeo Único
Deleção de Sequência
Neoplasias do Colo do Útero/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (GPI-Linked Proteins); 0 (Receptors, Tumor Necrosis Factor, Member 10c); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFRSF10C protein, human); 0 (TNFRSF10D protein, human); 0 (Tumor Necrosis Factor Decoy Receptors); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151107
[St] Status:MEDLINE
[do] DOI:10.1002/gcc.22325


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[PMID]:26390425
[Au] Autor:Beyer K; Normann L; Sendler M; Käding A; Heidecke CD; Partecke LI; von Bernstorff W
[Ad] Endereço:From the *Departments of General, Visceral, Thoracic and Vascular Surgery and †Medicine A (Gastroenterology and Nephrology), University Medicine Greifswald, Ernst-Moritz-Arndt-University, Greifswald, Germany.
[Ti] Título:TRAIL Promotes Tumor Growth in a Syngeneic Murine Orthotopic Pancreatic Cancer Model and Affects the Host Immune Response.
[So] Source:Pancreas;45(3):401-8, 2016 Mar.
[Is] ISSN:1536-4828
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is currently being evaluated as a possible biological agent for cancer treatment. However, many tumor cells are resistant to TRAIL-induced apoptosis. In these cases, TRAIL may activate different pathways promoting tumor growth as well as showing different interactions with the immunological tumor microenvironment. In this study, the impact of TRAIL on tumor growth and survival in a syngeneic model of TRAIL-resistant pancreatic cancer cells was investigated. METHODS: Murine 6606PDA pancreatic cancer cells were injected into the pancreatic heads of TRAIL mice and their littermates. To examine a direct effect of TRAIL on tumor cells, cultures of 6606PDA were TRAIL stimulated. RESULTS: The TRAIL mice displayed significantly decreased tumor volumes and an enhanced overall survival in pancreatic cancer. The decreased tumor growth in TRAIL mice was accompanied by a decrease of regulatory CD4 cells within tumors. Concordantly, TRAIL treatment of wild-type mice enhanced tumor growth and increased the fraction of regulatory CD4 cells. Yet, a direct effect of TRAIL on 6606PDA cells was not detected. CONCLUSIONS: Thus, TRAIL can promote tumor growth in TRAIL-resistant tumor cells. This may restrict possible future clinical applications of TRAIL in pancreatic cancer.
[Mh] Termos MeSH primário: Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Neoplasias Pancreáticas/tratamento farmacológico
Linfócitos T Reguladores/efeitos dos fármacos
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular Tumoral
Modelos Animais de Doenças
Resistência a Medicamentos Antineoplásicos/genética
Resistência a Medicamentos Antineoplásicos/imunologia
Seres Humanos
Estimativa de Kaplan-Meier
Células Matadoras Naturais/efeitos dos fármacos
Células Matadoras Naturais/imunologia
Células Matadoras Naturais/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/imunologia
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Membro 10c de Receptores do Fator de Necrose Tumoral/genética
Membro 10c de Receptores do Fator de Necrose Tumoral/metabolismo
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/metabolismo
Ligante Indutor de Apoptose Relacionado a TNF/genética
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Transplante Isogênico
Carga Tumoral/efeitos dos fármacos
Carga Tumoral/genética
Carga Tumoral/imunologia
Microambiente Tumoral/efeitos dos fármacos
Microambiente Tumoral/genética
Microambiente Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (Receptors, Tumor Necrosis Factor, Member 10c); 0 (TNF-Related Apoptosis-Inducing Ligand)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150922
[St] Status:MEDLINE
[do] DOI:10.1097/MPA.0000000000000469


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[PMID]:26050621
[Au] Autor:O'Leary L; van der Sloot AM; Reis CR; Deegan S; Ryan AE; Dhami SP; Murillo LS; Cool RH; Correa de Sampaio P; Thompson K; Murphy G; Quax WJ; Serrano L; Samali A; Szegezdi E
[Ad] Endereço:Apoptosis Research Centre, National University of Ireland, Galway, Ireland.
[Ti] Título:Decoy receptors block TRAIL sensitivity at a supracellular level: the role of stromal cells in controlling tumour TRAIL sensitivity.
[So] Source:Oncogene;35(10):1261-70, 2016 Mar 10.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is a death ligand cytokine known for its cytotoxic activity against malignantly transformed cells. TRAIL induces cell death through binding to death receptors DR4 and DR5. The inhibitory decoy receptors (DcR1 and DcR2) co-expressed with death receptor 4 (DR4)/DR5 on the same cell can block the transmission of the apoptotic signal. Here, we show that DcRs also regulate TRAIL sensitivity at a supracellular level and thus represent a mechanism by which the microenvironment can diminish tumour TRAIL sensitivity. Mathematical modelling and layered or spheroid stroma-extracellular matrix-tumour cultures were used to model the tumour microenvironment. By engineering TRAIL to escape binding by DcRs, we found that DcRs do not only act in a cell-autonomous or cis-regulatory manner, but also exert trans-cellular regulation originating from stromal cells and affect tumour cells, highlighting the potent inhibitory effect of DcRs in the tumour tissue and the necessity of selective targeting of the two death-inducing TRAIL receptors to maximise efficacy.
[Mh] Termos MeSH primário: Membro 10c de Receptores do Fator de Necrose Tumoral/metabolismo
Células Estromais/patologia
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Receptores Chamariz do Fator de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/metabolismo
Seres Humanos
Modelos Biológicos
Modelos Moleculares
Mutagênese Sítio-Dirigida
Mutação
Conformação Proteica
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética
Membro 10c de Receptores do Fator de Necrose Tumoral/genética
Células Estromais/metabolismo
Ligante Indutor de Apoptose Relacionado a TNF/química
Ligante Indutor de Apoptose Relacionado a TNF/genética
Receptores Chamariz do Fator de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GPI-Linked Proteins); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (Receptors, Tumor Necrosis Factor, Member 10c); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFRSF10C protein, human); 0 (TNFRSF10D protein, human); 0 (Tumor Necrosis Factor Decoy Receptors)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150609
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2015.180


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[PMID]:26514480
[Au] Autor:Sriraksa R; Limpaiboon T
[Ad] Endereço:Centre for Research and Development of Medical Diagnostic Laboratories, Faculty of Associated Medical Sciences, and Liver Fluke and Cholangiocarcinoma Research Center, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand E-mail : temduang@kku.ac.th.
[Ti] Título:TRAIL in Combination with Subtoxic 5-FU Effectively Inhibit Cell Proliferation and Induce Apoptosis in Cholangiocarcinoma Cells.
[So] Source:Asian Pac J Cancer Prev;16(16):6991-6, 2015.
[Is] ISSN:2476-762X
[Cp] País de publicação:Thailand
[La] Idioma:eng
[Ab] Resumo:In the past decade, the incidence and mortality rates of cholangiocarcinoma (CCA) have been increasing worldwide. The relatively low responsiveness of CCA to conventional chemotherapy leads to poor overall survival. Recently, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL or Apo2L) has emerged as the most promising anti-cancer therapeutic agent since it is able to selectively induce apoptosis of tumor cells but not normal cells. In this study, we aimed to investigate the therapeutic effect of TRAIL in CCA cell lines (M213, M214 and KKU100) compared with the immortal biliary cell line, MMNK1, either alone or in combination with a subtoxic dose of 5-fluorouracil (5-FU). We found that recombinant human TRAIL (rhTRAIL) was a potential agent which significantly inhibited cell proliferation and mediated caspase activities (caspases 8, 9 and 3/7) and apoptosis of CCA cells. The combined treatment of rhTRAIL and 5-FU effectively enhanced inhibition of CCA cell growth with a smaller effect on MMNK1. Our finding suggests TRAIL to be a novel anti-cancer therapeutic agent and advantage of its combination with a conventional chemotherapeutic drug for effective treatment of CCA.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Neoplasias dos Ductos Biliares/tratamento farmacológico
Colangiocarcinoma/tratamento farmacológico
Fluoruracila/farmacologia
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Caspases/genética
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Fluoruracila/administração & dosagem
Proteínas Ligadas por GPI/genética
Expressão Gênica/efeitos dos fármacos
Seres Humanos
RNA Mensageiro/metabolismo
Membro 10c de Receptores do Fator de Necrose Tumoral/genética
Ligante Indutor de Apoptose Relacionado a TNF/administração & dosagem
Receptores Chamariz do Fator de Necrose Tumoral/genética
Proteína Supressora de Tumor p53/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GPI-Linked Proteins); 0 (RNA, Messenger); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (Receptors, Tumor Necrosis Factor, Member 10c); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFRSF10A protein, human); 0 (TNFRSF10C protein, human); 0 (TNFRSF10D protein, human); 0 (Tumor Necrosis Factor Decoy Receptors); 0 (Tumor Suppressor Protein p53); EC 3.4.22.- (Caspases); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170308
[Lr] Data última revisão:
170308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151031
[St] Status:MEDLINE


  8 / 160 MEDLINE  
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[PMID]:26152738
[Au] Autor:Liu Y; Hawkins OE; Vilgelm AE; Pawlikowski JS; Ecsedy JA; Sosman JA; Kelley MC; Richmond A
[Ad] Endereço:Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, Tennessee. Department of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee. Division of Epidemiology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
[Ti] Título:Combining an Aurora Kinase Inhibitor and a Death Receptor Ligand/Agonist Antibody Triggers Apoptosis in Melanoma Cells and Prevents Tumor Growth in Preclinical Mouse Models.
[So] Source:Clin Cancer Res;21(23):5338-48, 2015 Dec 01.
[Is] ISSN:1078-0432
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Preclinical studies show that inhibition of aurora kinases in melanoma tumors induces senescence and reduces tumor growth, but does not cause tumor regression. Additional preclinical models are needed to identify agents that will synergize with aurora kinase inhibitors to induce tumor regression. EXPERIMENTAL DESIGN: We combined treatment with an aurora kinase A inhibitor, MLN8237, with agents that activate death receptors (Apo2L/TRAIL or death receptor 5 agonists) and monitored the ability of this treatment to induce tumor apoptosis and melanoma tumor regression using human cell lines and patient-derived xenograft (PDX) mouse models. RESULTS: We found that this combined treatment led to apoptosis and markedly reduced cell viability. Mechanistic analysis showed that the induction of tumor cell senescence in response to the AURKA inhibitor resulted in a decreased display of Apo2L/TRAIL decoy receptors and increased display of one Apo2L/TRAIL receptor (death receptor 5), resulting in enhanced response to death receptor ligand/agonists. When death receptors were activated in senescent tumor cells, both intrinsic and extrinsic apoptotic pathways were induced independent of BRAF, NRAS, or p53 mutation status. Senescent tumor cells exhibited BID-mediated mitochondrial depolarization in response to Apo2L/TRAIL treatment. In addition, senescent tumor cells had a lower apoptotic threshold due to decreased XIAP and survivin expression. Melanoma tumor xenografts of one human cell line and one PDX displayed total blockage of tumor growth when treated with MLN8237 combined with DR5 agonist antibody. CONCLUSIONS: These findings provide a strong rationale for combining senescence-inducing therapeutics with death receptor agonists for improved cancer treatment.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Aurora Quinases/antagonistas & inibidores
Inibidores de Proteínas Quinases/farmacologia
Receptores de Morte Celular/agonistas
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Azepinas/farmacologia
Caspases/metabolismo
Linhagem Celular Tumoral
Senescência Celular/efeitos dos fármacos
Modelos Animais de Doenças
Avaliação Pré-Clínica de Medicamentos
Feminino
Seres Humanos
Melanoma/tratamento farmacológico
Melanoma/genética
Melanoma/metabolismo
Melanoma/patologia
Camundongos
Pirimidinas/farmacologia
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Membro 10c de Receptores do Fator de Necrose Tumoral/metabolismo
Transdução de Sinais/efeitos dos fármacos
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[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 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 0 (Azepines); 0 (MLN 8237); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (Receptors, Death Domain); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (Receptors, Tumor Necrosis Factor, Member 10c); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (Tumor Suppressor Protein p53); EC 2.7.11.1 (Aurora Kinases); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150709
[St] Status:MEDLINE
[do] DOI:10.1158/1078-0432.CCR-15-0293


  9 / 160 MEDLINE  
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[PMID]:26111475
[Au] Autor:Shin D; Kwon HY; Sohn EJ; Nam MS; Kim JH; Lee JC; Ryu SY; Park B; Kim SH
[Ad] Endereço:College of Korean Medicine, Kyung Hee University, Seoul, South Korea.
[Ti] Título:Upregulation of Death Receptor 5 and Production of Reactive Oxygen Species Mediate Sensitization of PC-3 Prostate Cancer Cells to TRAIL Induced Apoptosis by Vitisin A.
[So] Source:Cell Physiol Biochem;36(3):1151-62, 2015.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Although Vitisin A, derived from wine grapes, is known to have cytotoxic, anti-adipogenic, anti-inflammatory and antioxidant effects, the underlying antitumor mechanism has not been investigated in prostate cancer cells to date. In the present study, the apoptotic mechanism of Vitisin A plus TNF-related apoptosis-inducing ligand (TRAIL) in prostate cancer cells was elucidated. METHODS: The cytotoxicity of Vitisin A and/or TRAIL against PC-3, DU145 and LNCaP prostate cancer cells was measured by MTT colorimetric assay. Annexin V-FITC Apoptosis Detection kit was used to detect apoptotic cells by flow cytometry. Intracellular levels of ROS were measured by flow cytometry using 2070-diacetyl dichlorofluorescein (DCFDA). RESULTS: Combined treatment with Vitisin A and TRAIL enhanced cytotoxicity and also increased sub-G1 population in PC-3 cells better than DU145 or LNCap prostate cancer cells. Similarly, Annexin V and PI staining revealed that combination increased early and late apoptosis in PC-3 cells compared to untreated control. Consistently, combination attenuated the expression of pro-caspases 7/8, DcR1, Bcl-XL or Bcl-2 and activated caspase 3, FADD, DR5 and DR4 in PC-3 cells. Also, combination increased DR5 promoter activity compared to untreated control. Furthermore, combination increased the production of reactive oxygen species (ROS) and DR5 cell surface expression. The ROS inhibitor NAC and silencing of DR5 by siRNA transfection inhibited the ability of combination to induce PARP cleavage and generate ROS. CONCLUSION: These findings provide evidence that Vitisin A can be used in conjunction with TRAIL as a potent TRAIL sensitizer for synergistic apoptosis induction via upregulation of DR5 and production of ROS in prostate cancer cells.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Benzofuranos/farmacologia
Regulação Neoplásica da Expressão Gênica
Fenóis/farmacologia
Próstata/efeitos dos fármacos
Espécies Reativas de Oxigênio/agonistas
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/agonistas
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Caspase 7/genética
Caspase 7/metabolismo
Caspase 8/genética
Caspase 8/metabolismo
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Combinação de Medicamentos
Sinergismo Farmacológico
Proteína de Domínio de Morte Associada a Fas/genética
Proteína de Domínio de Morte Associada a Fas/metabolismo
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/metabolismo
Seres Humanos
Masculino
Próstata/metabolismo
Próstata/patologia
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/antagonistas & inibidores
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Membro 10c de Receptores do Fator de Necrose Tumoral/genética
Membro 10c de Receptores do Fator de Necrose Tumoral/metabolismo
Transdução de Sinais
Proteína bcl-X/genética
Proteína bcl-X/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (BCL2 protein, human); 0 (BCL2L1 protein, human); 0 (Benzofurans); 0 (Drug Combinations); 0 (FADD protein, human); 0 (Fas-Associated Death Domain Protein); 0 (GPI-Linked Proteins); 0 (Phenols); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (Receptors, Tumor Necrosis Factor, Member 10c); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFRSF10A protein, human); 0 (TNFRSF10C protein, human); 0 (TNFSF10 protein, human); 0 (bcl-X Protein); 142449-89-6 (vitisin A); EC 3.4.22.- (Caspase 7); EC 3.4.22.- (Caspase 8)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150707
[Lr] Data última revisão:
150707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150627
[St] Status:MEDLINE
[do] DOI:10.1159/000430286


  10 / 160 MEDLINE  
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[PMID]:25808868
[Au] Autor:Mansour NM; Bernal GM; Wu L; Crawley CD; Cahill KE; Voce DJ; Balyasnikova IV; Zhang W; Spretz R; Nunez L; Larsen GF; Weichselbaum RR; Yamini B
[Ad] Endereço:Department of Surgery, Section of Neurosurgery, The University of Chicago, Chicago, Illinois.
[Ti] Título:Decoy Receptor DcR1 Is Induced in a p50/Bcl3-Dependent Manner and Attenuates the Efficacy of Temozolomide.
[So] Source:Cancer Res;75(10):2039-48, 2015 May 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Temozolomide is used widely to treat malignant glioma, but the overall response to this agent is generally poor. Resistance to DNA-damaging drugs such as temozolomide has been related to the induction of antiapoptotic proteins. Specifically, the transcription factor NF-κB has been suggested to participate in promoting the survival of cells exposed to chemotherapy. To identify factors that modulate cytotoxicity in the setting of DNA damage, we used an unbiased strategy to examine the NF-κB-dependent expression profile induced by temozolomide. By this route, we defined the decoy receptor DcR1 as a temozolomide response gene induced by a mechanism relying upon p50/NF-κB1. A conserved NF-κB-binding sequence (κB-site) was identified in the proximal promoter and was demonstrated to be required for DcR1 induction by temozolomide. Loss-of-function and gain-of-function studies reveal that the atypical IκB protein, Bcl3, is also required for induction of DcR1 by temozolomide. Mechanistically, DcR1 attenuates temozolomide efficacy by blunting activation of the Fas receptor pathway in p53(+/+) glioma cells. Intracranial xenograft studies show that DcR1 depletion in glioma cells enhances the efficacy of temozolomide. Taken together, our results show how DcR1 upregulation mediates temozolomide resistance and provide a rationale for DcR1 targeting as a strategy to sensitize gliomas to this widely used chemotherapy.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Dacarbazina/análogos & derivados
Subunidade p50 de NF-kappa B/metabolismo
Proteínas Proto-Oncogênicas/metabolismo
Fatores de Transcrição/metabolismo
Receptores Chamariz do Fator de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Sítios de Ligação
Linhagem Celular Tumoral
Dacarbazina/farmacologia
Resistência a Medicamentos Antineoplásicos
Proteínas Ligadas por GPI/química
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/metabolismo
Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Glioma/tratamento farmacológico
Glioma/metabolismo
Seres Humanos
Masculino
Camundongos Nus
Regiões Promotoras Genéticas
Ligação Proteica
Membro 10c de Receptores do Fator de Necrose Tumoral
Ativação Transcricional
Receptores Chamariz do Fator de Necrose Tumoral/química
Receptores Chamariz do Fator de Necrose Tumoral/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (GPI-Linked Proteins); 0 (NF-kappa B p50 Subunit); 0 (Proto-Oncogene Proteins); 0 (Receptors, Tumor Necrosis Factor, Member 10c); 0 (TNFRSF10C protein, human); 0 (Transcription Factors); 0 (Tumor Necrosis Factor Decoy Receptors); 0 (proto-oncogene protein bcl-3); 7GR28W0FJI (Dacarbazine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150327
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-14-2144



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