Base de dados : MEDLINE
Pesquisa : D12.776.543.750.705.852.760.974 [Categoria DeCS]
Referências encontradas : 291 [refinar]
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  1 / 291 MEDLINE  
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[PMID]:28934756
[Au] Autor:Wang X; Xiao S; Xia Y
[Ti] Título:Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling.
[So] Source:Cell Physiol Biochem;43(2):579-588, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor (TNF)-related weak inducer of apoptosis (TWEAK) engages its sole receptor, fibroblast growth factor-inducible 14 (Fn14), which participates in various inflammatory and immunologic processes. TWEAK/Fn14 interaction induces different cell fates depending on the local microenvironment, which correlates with certain expression profiles of TNF receptors (TNFR). The predominant expression of TNFR1 or TNFR2 facilitates cell death or proliferation, respectively, on TWEAK/Fn14 activation. TNFR-associated factors (TRAF) interact with Fn14, cellular inhibitor of apoptosis protein (cIAP)-1, and TNFR, consequently transducing signals from TWEAK to downstream cytokines and cell cycle mediators. An Fn14-TRAF2-TNFR axis has been suggested in the function of TWEAK/Fn14 signaling, which may serve as a target in the development of novel therapeutic strategies for many diseases that have Fn14-overexpressing cells in affected tissues. The aims of this review are: 1) to present the main results on TWEAK/Fn14 regulation of cell fates, 2) to analyze the mechanism of the Fn14-TRAF2-TNFR axis, and 3) to summarize the potential strategies in the pharmacologic targeting of this axis.
[Mh] Termos MeSH primário: Inflamação/imunologia
Receptores do Fator de Necrose Tumoral/imunologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Inflamação/tratamento farmacológico
Terapia de Alvo Molecular
Mapas de Interação de Proteínas/efeitos dos fármacos
Receptores do Fator de Necrose Tumoral/análise
Transdução de Sinais/efeitos dos fármacos
Receptor de TWEAK
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Tumor Necrosis Factor); 0 (TNFRSF12A protein, human); 0 (TWEAK Receptor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1159/000480530


  2 / 291 MEDLINE  
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[PMID]:28715634
[Au] Autor:Li Z; Xie J; Peng S; Liu S; Wang Y; Lu W; Shen J; Li C
[Ad] Endereço:College of Pharmaceutical Sciences, Southwest University , Chongqing, 400715, PR China.
[Ti] Título:Novel Strategy Utilizing Extracellular Cysteine-Rich Domain of Membrane Receptor for Constructing d-Peptide Mediated Targeted Drug Delivery Systems: A Case Study on Fn14.
[So] Source:Bioconjug Chem;28(8):2167-2179, 2017 Aug 16.
[Is] ISSN:1520-4812
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The development of proteolysis-resistant d-peptide ligands for targeted drug/gene delivery has been greatly limited, due to the challenge that lies in the chemical synthesis of membrane receptors without altering their structures. In the present research, a novel strategy utilizing self-stabilized extracellular CRD of the membrane receptor was developed to construct d-peptide ligands and their mediated targeted drug delivery systems. Fn14, a cell surface receptor overexpressed in many cancers including pancreatic and triple-negative breast cancers, was selected as the model receptor. Fn14 CRD was synthesized and folded, and used to screen Fn14 binding peptides using phage display (l-peptide) and mirror-image phage display (d-peptide) techniques, respectively. The d-peptide ligand successfully mediated targeted drug delivery to Fn14 positive tumor cells. In addition, the d-peptide possessed better target-binding affinity, stromal barrier permeability, and tumor targeting ability in vivo when conjugated with liposomes. More importantly, d-peptide mediated liposomal paclitaxel delivery significantly inhibited pancreatic tumor growth in a subcutaneous xenograft model and drastically prolonged survival in a lung metastasis of breast cancer mouse model. This study demonstrated that mirror-image phage display based on the CRD of membrane receptor can be a promising strategy to advance active targeted drug delivery via biostable d-peptides.
[Mh] Termos MeSH primário: Cisteína/química
Portadores de Fármacos/química
Portadores de Fármacos/metabolismo
Espaço Extracelular/metabolismo
Peptídeos/química
Peptídeos/metabolismo
Receptores do Fator de Necrose Tumoral/química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Linhagem Celular Tumoral
Seres Humanos
Camundongos
Modelos Moleculares
Células NIH 3T3
Domínios Proteicos
Receptor de TWEAK
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Carriers); 0 (Peptides); 0 (Receptors, Tumor Necrosis Factor); 0 (TNFRSF12A protein, human); 0 (TWEAK Receptor); 0 (Tnfrsf12a protein, mouse); K848JZ4886 (Cysteine)
[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:170718
[St] Status:MEDLINE
[do] DOI:10.1021/acs.bioconjchem.7b00326


  3 / 291 MEDLINE  
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[PMID]:28639899
[Au] Autor:Hu G; Zeng W; Xia Y
[Ad] Endereço:Department of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
[Ti] Título:TWEAK/Fn14 signaling in tumors.
[So] Source:Tumour Biol;39(6):1010428317714624, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TWEAK (tumor necrosis factor-related weak inducer of apoptosis), a member of the tumor necrosis factor superfamily, acts on cells by binding to its only receptor named Fn14 (fibroblast growth factor-inducible 14). Their engagement activates a number of intracellular signal transduction cascades and consequently leads to cell death, proliferation, migration, or survival depending on the cellular contexts. Studies have indicated that the expression of TWEAK and Fn14 is upregulated in many solid tumors compared with healthy tissues. The activation of TWEAK/Fn14 signaling enhances the proliferation, invasion, and migration of tumor cells. Moreover, the angiogenesis, pro-inflammatory cytokine expression, and epithelial-mesenchymal transitions are promoted upon TWEAK/Fn14 activation. Currently, the tumor necrosis factor receptor-associated factor and nuclear factor kappa B signaling pathways are considered two main downstream pathways activated by TWEAK/Fn14 interaction. In view of these facts, some TWEAK- or Fn14-targeting agents are generated to inhibit the progression of tumors and have achieved initial success in clinical and pre-clinical trials. These agents include monoclonal antibodies, fusion proteins, immunotoxins, and nanoparticles. In addition, some relevant signaling pathways are studied to identify new potential therapeutic targets. Overall, these findings suggest that the TWEAK/Fn14 pathway is critical in the development of tumors, and targeting this signaling is a potential therapeutic approach in future tumor therapy.
[Mh] Termos MeSH primário: Neoplasias/genética
Receptores do Fator de Necrose Tumoral/genética
Fatores de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Movimento Celular/genética
Proliferação Celular/genética
Citocina TWEAK
Seres Humanos
Invasividade Neoplásica/genética
Neoplasias/patologia
Transdução de Sinais
Receptor de TWEAK
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokine TWEAK); 0 (Receptors, Tumor Necrosis Factor); 0 (TNFRSF12A protein, human); 0 (TNFSF12 protein, human); 0 (TWEAK Receptor); 0 (Tumor Necrosis Factors)
[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:170623
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317714624


  4 / 291 MEDLINE  
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[PMID]:28411440
[Au] Autor:Wang A; Zhang F; Xu H; Xu M; Cao Y; Wang C; Xu Y; Su M; Zhang M; Zhuge Y
[Ad] Endereço:Department of Gastroenterology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, Jiangsu, China.
[Ti] Título:TWEAK/Fn14 promotes pro-inflammatory cytokine secretion in hepatic stellate cells via NF-κB/STAT3 pathways.
[So] Source:Mol Immunol;87:67-75, 2017 Jul.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) have been associated with liver disease. Hepatic stellate cells (HSCs) play a critical role in the hepatic wound-healing response after liver injury, but there is little information available on the role of the TWEAK/Fn14 pathway in human HSCs. In this study, we explored the role of TWEAK/Fn14 in activated human HSCs. The LX-2 cells were treated with TWEAK, and the expression of pro-inflammatory cytokines was assayed by enzyme-linked immunosorbent assay (ELISA) and real-time PCR (RT-PCR). Western blotting and RT-PCR were performed to evaluate the expression of Fn14 after TWEAK stimulation. Total and phosphorylated of inhibitor-κB (I-κB), nuclear factor kappa B (NF-κB), Janus kinase 2 (JAK2), and signal transducers and activators of transcription 3 (STAT3) were examined by western blotting after TWEAK stimulation and small interfering RNA (siRNA) transfection. The result showed that TWEAK upregulated the expression of Fn14 and pro-inflammatory factors interleukin-8 (IL-8), interleukin-6 (IL-6), regulated upon activation normal T cell expressed and secreted (RANTES), and monocyte chemotactic protein-1 (MCP-1). In LX-2 cells, the pro-inflammatory cytokine secretion was closely related to the activation of the NF-κB and STAT3 pathways. Furthermore, our research showed that STAT3 and NF-κB could interact with each other, which resulted in a significant increase of pro-inflammatory cytokine secretion. The activation of NF-κB and STAT3 signalling-dependent pro-inflammatory cytokine expression may be responsible for such a novel principle and new therapeutic targets in chronic liver disease.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Células Estreladas do Fígado/metabolismo
Inflamação/metabolismo
NF-kappa B/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
Fator de Transcrição STAT3/metabolismo
Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Células Cultivadas
Quimiocina CCL2/metabolismo
Citocina TWEAK
Seres Humanos
Interleucina-6/metabolismo
Interleucina-8/metabolismo
Janus Quinase 2/metabolismo
RNA Interferente Pequeno/genética
Transdução de Sinais/fisiologia
Receptor de TWEAK
Fator de Necrose Tumoral alfa/metabolismo
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Cytokine TWEAK); 0 (Cytokines); 0 (Interleukin-6); 0 (Interleukin-8); 0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (Receptors, Tumor Necrosis Factor); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (TNFRSF12A protein, human); 0 (TNFSF12 protein, human); 0 (TWEAK Receptor); 0 (Tumor Necrosis Factor-alpha); 0 (Tumor Necrosis Factors); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2)
[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:170416
[St] Status:MEDLINE


  5 / 291 MEDLINE  
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[PMID]:28357912
[Au] Autor:Keshtvarz M; Salimian J; Yaseri M; Bathaie SZ; Rezaie E; Aliramezani A; Norouzbabaei Z; Amani J; Douraghi M
[Ad] Endereço:Division of Microbiology, Department of Pathobiology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
[Ti] Título:Bioinformatic prediction and experimental validation of a PE38-based recombinant immunotoxin targeting the Fn14 receptor in cancer cells.
[So] Source:Immunotherapy;9(5):387-400, 2017 Mar.
[Is] ISSN:1750-7448
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: AFn14R can serve as an ideal target for cancer immunotherapy. Here, a combined bioinformatic and experimental approach was applied to characterize an immunotoxin consisting of single-chain variable fragment antibody that targets Fn14 and a toxin fragment (PE38). METHODS & RESULTS: Flow cytometry results showed that the rate of PE38-P4A8 binding to Fn14 was approximately 60 and 40% in HT-29 and A549 cells, respectively. Moreover, 1 ng/µl of immunotoxin was able to lyse approximately 53 and 41% of HT-29 and A549, respectively. PE38-P4A8 showed stability in mouse serum (∼90%) after 3-h incubation. Most importantly, using bioinformatics for determining the structure and function of fusion proteins can be very helpful in designing of experiments. CONCLUSION: Coupled with bioinformatics, experimental approaches revealed that PE38-P4A8 could be used as a promising therapeutic agent for cancer cells expressing Fn14.
[Mh] Termos MeSH primário: Adenocarcinoma/terapia
Antígenos de Neoplasias/metabolismo
Biologia Computacional
Receptores do Fator de Necrose Tumoral/metabolismo
Anticorpos de Cadeia Única/metabolismo
[Mh] Termos MeSH secundário: Células A549
Seres Humanos
Imunotoxinas/genética
Imunotoxinas/metabolismo
Terapia de Alvo Molecular
Proteínas Recombinantes de Fusão/genética
Anticorpos de Cadeia Única/genética
Receptor de TWEAK
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Immunotoxins); 0 (Receptors, Tumor Necrosis Factor); 0 (Recombinant Fusion Proteins); 0 (Single-Chain Antibodies); 0 (TNFRSF12A protein, human); 0 (TWEAK Receptor); 0 (Tnfrsf12a protein, mouse)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.2217/imt-2017-0008


  6 / 291 MEDLINE  
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[PMID]:28351660
[Au] Autor:Liu Y; Peng L; Li L; Liu C; Hu X; Xiao S; Xia Y
[Ad] Endereço:Department of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
[Ti] Título:TWEAK/Fn14 Activation Contributes to the Pathogenesis of Bullous Pemphigoid.
[So] Source:J Invest Dermatol;137(7):1512-1522, 2017 Jul.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TWEAK participates in various cellular effects by engaging its receptor of Fn14. Increased levels of soluble TWEAK are associated with systemic autoimmunity in patients with lupus erythematosus, rheumatoid arthritis, or dermatomyositis. However, the role of TWEAK in bullous pemphigoid (BP) remains unknown. In this study, we found an elevated serum level of TWEAK and a positive correlation between serum TWEAK and anti-BP180 antibodies. Immunohistochemistry showed strong TWEAK and Fn14 expression and implied an opposite relationship between the TWEAK and BP180 expression in skin samples from BP patients. In vitro TWEAK stimuli reduced BP180 expression in HaCaT cells and inhibited the adhesion of cells to the culture dish. Consistently, the transfection of Fn14 small interfering RNA preserved BP180 and protected cells from losing adherence. Moreover, such effect of TWEAK correlated with activation of the extracellular signal-regulated kinase and NF-κB pathways and downstream ADAMs. By silencing ADAM17 with small interfering RNA, we showed that ADAM17 participated in TWEAK-induced BP180 loss. Therefore, TWEAK may contribute to the pathogenesis of BP by reducing BP180 expression and cellular adherence, involving the activation of ERK and NF-κB pathways. TWEAK may serve as a biomarker or therapeutic target of BP.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Penfigoide Bolhoso/genética
RNA/genética
Receptores do Fator de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Western Blotting
Células Cultivadas
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Imuno-Histoquímica
Queratinócitos/metabolismo
Queratinócitos/patologia
NF-kappa B/metabolismo
Penfigoide Bolhoso/metabolismo
Penfigoide Bolhoso/patologia
Receptores do Fator de Necrose Tumoral/biossíntese
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais
Receptor de TWEAK
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Receptors, Tumor Necrosis Factor); 0 (TNFRSF12A protein, human); 0 (TWEAK Receptor); 63231-63-0 (RNA)
[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:170330
[St] Status:MEDLINE


  7 / 291 MEDLINE  
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[PMID]:28180936
[Au] Autor:Zheng L; Lv Z; Gong Z; Sheng Q; Gao Z; Zhang Y; Yu S; Zhou J; Xi Z; Wang X
[Ad] Endereço:Department of Pediatric Surgery, Shanghai Children's Hospital, Shanghai Jiao Tong University, No. 355 Luding Road, Shanghai, 200062, China.
[Ti] Título:Fn14 hepatic progenitor cells are associated with liver fibrosis in biliary atresia.
[So] Source:Pediatr Surg Int;33(5):593-599, 2017 May.
[Is] ISSN:1437-9813
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The liver in biliary atresia (BA) is characterized by progressing fibrosis which is promoted by unclear reasons. We aimed to understand the factors influencing liver fibrosis. This study hypothesized that HPCs (hepatic progenitor cells) are activated and associated with liver fibrosis in biliary atresia. METHODS: Liver samples from biliary atresia patients are as BA group, and the normal liver derived from hepatoblastoma infants during operation are control group. The extent of fibrosis in liver samples was blindly evaluated by two experienced pathologists depending on Ishak system. The BA liver samples were divided into mild liver fibrosis group (grade I-IV, BA ) and severe liver fibrosis group (grade V-VI, BA ) to detect Fn14 protein expression. RESULTS: In mRNA level, Fn14 expression was 21.23 ± 8.3 vs. 1.00 ± 0.17, p = 0.023 < 0.05 and CD133 expression was 6.02 ± 2.16 vs. 1.14 ± 0.75, p = 0.008 < 0.01 between BA group and control group. Fn14 cells co-expressed the progenitor marker CD133 in liver, and activated in BA. Fn14 andα-SMA were co-location in fibrous area in liver. Compared to the control group, Fn14, CD133, and α-SMA protein expression were 2.10 ± 0.53 vs. 0.97 ± 0.2, p = 0.001, 2.23 ± 0.57 vs. 1.00 ± 0.03, p = 0.000, 4.96 ± 2.4 vs. 1.00 ± 0.22, p = 0.001. The Fn14 protein expression was 2.60 ± 0.35 vs. 1.86 ± 0.42, p = 0.012, between BA and BA group. CONCLUSION: Fn14 cells, which co-express the progenitor marker CD133 in liver, are HPCs and activated in BA. Fn14 + HPCs are associated with liver fibrosis in BA.
[Mh] Termos MeSH primário: Atresia Biliar/complicações
Atresia Biliar/metabolismo
Cirrose Hepática/complicações
Cirrose Hepática/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Atresia Biliar/cirurgia
Biomarcadores/metabolismo
Criança
Pré-Escolar
Seres Humanos
Lactente
Fígado/metabolismo
Cirrose Hepática/genética
Testes de Função Hepática
Masculino
Receptores do Fator de Necrose Tumoral/genética
Receptor de TWEAK
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Receptors, Tumor Necrosis Factor); 0 (TNFRSF12A protein, human); 0 (TWEAK Receptor)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170210
[St] Status:MEDLINE
[do] DOI:10.1007/s00383-017-4068-5


  8 / 291 MEDLINE  
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[PMID]:28138696
[Au] Autor:Wang T; Ma S; Qi X; Tang X; Cui D; Wang Z; Chi J; Li P; Zhai B
[Ad] Endereço:Department of Interventional Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, P.R. China.
[Ti] Título:Knockdown of the differentially expressed gene TNFRSF12A inhibits hepatocellular carcinoma cell proliferation and migration in vitro.
[So] Source:Mol Med Rep;15(3):1172-1178, 2017 Mar.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Human hepatocellular carcinoma (HCC) has been reported to be highly insensitive to conventional chemotherapy. In the current study, the Agilent Whole Human Genome Oligo Microarray (4x44 K) was used in order to identify the differentially expressed genes between HCC and adjacent tissues, and the top 22 differentially expressed genes were confirmed through reverse transcription­quantitative polymerase chain reaction. Among the identified differences in gene expression, expression of tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) was markedly higher in HCC tissue than in adjacent tissue. Previous studies have suggested that TNFRSF12A may serve a role in tumor growth and metastasis, thus in the current study, TNFRSF12A was knocked down in the SMMC7721 cell line through siRNA. This demonstrated that cells exhibited reduced reproductive and metastatic capacity ex vivo. Thus, the results of the current study suggest that TNFRSF12A may be a candidate therapeutic target for cancer including HCC, and additional genes that exhibited significantly different expression from normal adjacent tissues require further study.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Regulação Neoplásica da Expressão Gênica
Neoplasias Hepáticas/genética
Receptores do Fator de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/patologia
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular
Sobrevivência Celular/genética
Análise por Conglomerados
Biologia Computacional/métodos
Perfilação da Expressão Gênica
Técnicas de Silenciamento de Genes
Seres Humanos
Neoplasias Hepáticas/patologia
Receptor de TWEAK
Transcriptoma
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Tumor Necrosis Factor); 0 (TNFRSF12A protein, human); 0 (TWEAK Receptor)
[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:170201
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2017.6154


  9 / 291 MEDLINE  
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[PMID]:28103571
[Au] Autor:Roos A; Dhruv HD; Mathews IT; Inge LJ; Tuncali S; Hartman LK; Chow D; Millard N; Yin HH; Kloss J; Loftus JC; Winkles JA; Berens ME; Tran NL
[Ad] Endereço:Department of Cancer Biology, Mayo Clinic Arizona, Scottsdale, Arizona 85259, USA.
[Ti] Título:Identification of aurintricarboxylic acid as a selective inhibitor of the TWEAK-Fn14 signaling pathway in glioblastoma cells.
[So] Source:Oncotarget;8(7):12234-12246, 2017 Feb 14.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The survival of patients diagnosed with glioblastoma (GBM), the most deadly form of brain cancer, is compromised by the proclivity for local invasion into the surrounding normal brain, which prevents complete surgical resection and contributes to therapeutic resistance. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK), a member of the tumor necrosis factor (TNF) superfamily, can stimulate glioma cell invasion and survival via binding to fibroblast growth factor-inducible 14 (Fn14) and subsequent activation of the transcription factor NF-κB. To discover small molecule inhibitors that disrupt the TWEAK-Fn14 signaling axis, we utilized a cell-based drug-screening assay using HEK293 cells engineered to express both Fn14 and a NF-κB-driven firefly luciferase reporter protein. Focusing on the LOPAC1280 library of 1280 pharmacologically active compounds, we identified aurintricarboxylic acid (ATA) as an agent that suppressed TWEAK-Fn14-NF-κB dependent signaling, but not TNFα-TNFR-NF-κB driven signaling. We demonstrated that ATA repressed TWEAK-induced glioma cell chemotactic migration and invasion via inhibition of Rac1 activation but had no effect on cell viability or Fn14 expression. In addition, ATA treatment enhanced glioma cell sensitivity to both the chemotherapeutic agent temozolomide (TMZ) and radiation-induced cell death. In summary, this work reports a repurposed use of a small molecule inhibitor that targets the TWEAK-Fn14 signaling axis, which could potentially be developed as a new therapeutic agent for treatment of GBM patients.
[Mh] Termos MeSH primário: Ácido Aurintricarboxílico/farmacologia
Neoplasias Encefálicas/tratamento farmacológico
Glioblastoma/tratamento farmacológico
Receptores do Fator de Necrose Tumoral/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Alquilantes/farmacologia
Ácido Aurintricarboxílico/química
Neoplasias Encefálicas/genética
Neoplasias Encefálicas/metabolismo
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Movimento Celular/genética
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Sobrevivência Celular/efeitos da radiação
Citocina TWEAK
Dacarbazina/análogos & derivados
Dacarbazina/farmacologia
Sinergismo Farmacológico
Glioblastoma/genética
Glioblastoma/metabolismo
Células HEK293
Seres Humanos
Estimativa de Kaplan-Meier
Camundongos Nus
Estrutura Molecular
Interferência de RNA
Receptores do Fator de Necrose Tumoral/genética
Transdução de Sinais/genética
Bibliotecas de Moléculas Pequenas/química
Bibliotecas de Moléculas Pequenas/farmacologia
Receptor de TWEAK
Fatores de Necrose Tumoral/genética
Ensaios Antitumorais Modelo de Xenoenxerto/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Cytokine TWEAK); 0 (Receptors, Tumor Necrosis Factor); 0 (Small Molecule Libraries); 0 (TNFRSF12A protein, human); 0 (TNFSF12 protein, human); 0 (TWEAK Receptor); 0 (Tnfrsf12a protein, mouse); 0 (Tumor Necrosis Factors); 4431-00-9 (Aurintricarboxylic Acid); 7GR28W0FJI (Dacarbazine); YF1K15M17Y (temozolomide)
[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:170120
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.14685


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[PMID]:27888541
[Au] Autor:Zhang F; Zhang M; Wang A; Xu M; Wang C; Xu G; Zhang B; Zou X; Zhuge Y
[Ad] Endereço:Department of Gastroenterology, Affiliated Drum Tower Hospital of Nanjing University Medical School, 321# Zhongshan Road, Nanjing 210008, Jiangsu, China.
[Ti] Título:TWEAK increases SIRT1 expression and promotes p53 deacetylation affecting human hepatic stellate cell senescence.
[So] Source:Cell Biol Int;41(2):147-154, 2017 Feb.
[Is] ISSN:1095-8355
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To detect the effects of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) on SIRT1 expression and p53 deacetylation, involving cell senescence, in activated human hepatic stellate cell (HSC) in vitro, human HSC LX-2 was cultured with TWEAK for 24 h. The result showed that the expression of membrane receptor Fn14 was remarkably increased by TWEAK, which upregulated SIRT1 in LX-2 cells, detected by Western blotting and real-time PCR. The expression of p53 was not significantly altered; however, the ac-p53 was decreased. Furthermore, the viability of LX-2 cells was significantly enhanced by TWEAK. The activity of SA-ß-Gal was notably inhibited, showing a suppressing effect of TWEAK on the senescence of activated HSC. Primary cultured HSC on days 7 and 11 was used to examine the expression of TWEAK, Fn14, SIRT1, and the activity of SA-ß-Gal. The result indicated that the mRNA of TWEAK, SIRT1, and Fn14 was all decreased on day 11 compared to that on day 7, and the activity of SA-ß-Gal was higher on day 11 than that on day 7. The present study suggested that TWEAK enhanced the expression of SIRT1 and decreased the acetylation of p53, probably inhibiting the senescence of activated HSC in vitro, which provides a molecular basis for TWEAK as a potential target in the therapy of liver fibrosis.
[Mh] Termos MeSH primário: Senescência Celular/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Sirtuína 1/genética
Fatores de Necrose Tumoral/farmacologia
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Acetilação/efeitos dos fármacos
Actinas/genética
Actinas/metabolismo
Animais
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Citocina TWEAK
Células Estreladas do Fígado/citologia
Células Estreladas do Fígado/metabolismo
Cirrose Hepática/metabolismo
Cirrose Hepática/patologia
Masculino
Camundongos
RNA Mensageiro/metabolismo
Receptores do Fator de Necrose Tumoral/genética
Receptores do Fator de Necrose Tumoral/metabolismo
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/isolamento & purificação
Proteínas Recombinantes/farmacologia
Sirtuína 1/metabolismo
Receptor de TWEAK
Fatores de Necrose Tumoral/genética
Fatores de Necrose Tumoral/metabolismo
Proteína Supressora de Tumor p53/genética
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Cytokine TWEAK); 0 (RNA, Messenger); 0 (Receptors, Tumor Necrosis Factor); 0 (Recombinant Proteins); 0 (TNFRSF12A protein, human); 0 (TWEAK Receptor); 0 (Tnfrsf12a protein, mouse); 0 (Tnfsf12 protein, mouse); 0 (Tumor Necrosis Factors); 0 (Tumor Suppressor Protein p53); 0 (alpha-smooth muscle actin, mouse); EC 3.5.1.- (Sirtuin 1)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161127
[St] Status:MEDLINE
[do] DOI:10.1002/cbin.10706



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