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  1 / 5059 MEDLINE  
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[PMID]:28460464
[Au] Autor:Nazim UM; Moon JH; Lee YJ; Seol JW; Park SY
[Ad] Endereço:Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Jeonbuk 54596, South Korea.
[Ti] Título:PPARγ activation by troglitazone enhances human lung cancer cells to TRAIL-induced apoptosis via autophagy flux.
[So] Source:Oncotarget;8(16):26819-26831, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Members of the tumor necrosis factor (TNF) transmembrane cytokine superfamily, such as TNFα and Fas ligand (FasL), play crucial roles in inflammation and immunity. TRAIL is a member of this superfamily with the ability to selectively trigger cancer cell death but does not motive cytotoxicity to most normal cells. Troglitazone are used in the cure of type II diabetes to reduce blood glucose levels and improve the sensitivity of an amount of tissues to insulin. In this study, we revealed that troglitazone could trigger TRAIL-mediated apoptotic cell death in human lung adenocarcinoma cells. Pretreatment of troglitazone induced activation of PPARγ in a dose-dependent manner. In addition conversion of LC3-I to LC3-II and PPARγ was suppressed in the presence of GW9662, a well-characterized PPARγ antagonist. Treatment with troglitazone resulted in a slight increase in conversion rate of LC3-I to LC3-II and significantly decreased p62 expression levels in a dose-dependent manner. This indicates that troglitazone induced autophagy flux activation in human lung cancer cells. Inhibition of autophagy flux applying a specific inhibitor and genetically modified ATG5 siRNA enclosed troglitazone-mediated enhancing effect of TRAIL. These data demonstrated that activation of PPARγ mediated by troglitazone enhances human lung cancer cells to TRAIL-induced apoptosis via autophagy flux and also suggest that troglitazone may be a combination therapeutic target with TRAIL protein in TRAIL-resistant cancer cells.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Cromanos/farmacologia
Neoplasias Pulmonares/metabolismo
PPAR gama/agonistas
PPAR gama/metabolismo
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
Tiazolidinedionas/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromans); 0 (PPAR gamma); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (Thiazolidinediones); I66ZZ0ZN0E (troglitazone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15819


  2 / 5059 MEDLINE  
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[PMID]:29374163
[Au] Autor:Márquez-Jurado S; Díaz-Colunga J; das Neves RP; Martinez-Lorente A; Almazán F; Guantes R; Iborra FJ
[Ad] Endereço:Department of Molecular and Cell Biology, Centro Nacional de Biotecnología (CNB-CSIC), Campus de Cantoblanco, 28049, Madrid, Spain.
[Ti] Título:Mitochondrial levels determine variability in cell death by modulating apoptotic gene expression.
[So] Source:Nat Commun;9(1):389, 2018 01 26.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fractional killing is the main cause of tumour resistance to chemotherapy. This phenomenon is observed even in genetically identical cancer cells in homogeneous microenvironments. To understand this variable resistance, here we investigate the individual responses to TRAIL in a clonal population of HeLa cells using live-cell microscopy and computational modelling. We show that the cellular mitochondrial content determines the apoptotic fate and modulates the time to death, cells with higher mitochondrial content are more prone to die. We find that all apoptotic protein levels are modulated by the mitochondrial content. Modelling the apoptotic network, we demonstrate that these correlations, and especially the differential control of anti- and pro-apoptotic protein pairs, confer mitochondria a powerful discriminatory capacity of apoptotic fate. We find a similar correlation between the mitochondria and apoptotic proteins in colon cancer biopsies. Our results reveal a different role of mitochondria in apoptosis as the global regulator of apoptotic protein expression.
[Mh] Termos MeSH primário: Apoptose/genética
Expressão Gênica/genética
Mitocôndrias/genética
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Algoritmos
Apoptose/efeitos dos fármacos
Proteínas Reguladoras de Apoptose/genética
Proteínas Reguladoras de Apoptose/metabolismo
Morte Celular/genética
Expressão Gênica/efeitos dos fármacos
Células HeLa
Seres Humanos
Mitocôndrias/metabolismo
Modelos Genéticos
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (Reactive Oxygen Species); 0 (TNF-Related Apoptosis-Inducing Ligand)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180128
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02787-4


  3 / 5059 MEDLINE  
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[PMID]:29305260
[Au] Autor:Xu Y; Gao CC; Pan ZG; Zhou CW
[Ad] Endereço:Huai'an First People's Hospital, Nanjing Medical University, No.6, Beijing West Road, Huai'an, 223300, China.
[Ti] Título:Irigenin sensitizes TRAIL-induced apoptosis via enhancing pro-apoptotic molecules in gastric cancer cells.
[So] Source:Biochem Biophys Res Commun;496(3):998-1005, 2018 02 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) holds promising value for cancer therapy due to its capacity to induce apoptosis in cancer cells. Nevertheless, TRAIL therapy is greatly hampered by its resistance. Irigenin (Iri), isoflavonoids, can be isolated from the rhizome of Belamcanda chinensis, and has been shown anti-cancer properties. In this study, we explored if Iri could enhance TRAIL-regulated apoptosis in TRAIL resistant gastric cancer cells. Iri significantly potentiated TRAIL-triggered cytotoxicity. Iri alone and TRAIL alone showed no effective role in apoptosis induction, whereas combined treatment with Iri and TRAIL markedly induced apoptosis in cancer cells, as evidenced by the up-regulation of cleaved Caspase-8/-9/-3 and PARP. Additionally, the sensitization to TRAIL was along with the enhancement of pro-apoptotic proteins, including FAS-associated protein with death domain (FADD), death receptor 5 (DR5) and Bax. And suppressing FADD, DR5 and Bax by si RNA significantly reduced the apoptosis and enhanced the cell viability induced by the co-application of Iri and TRAIL. Moreover, the sensitization to TRAIL was accompanied by the decrease of Cellular-FLICE inhibitory protein (c-FLIP), Bcl-2 and Survivin. Additionally, Iri could sensitize TRAIL to produce reactive oxygen species (ROS). Pre-treatment of N-acetyl-cysteine (NAC), ROS scavenger, attenuated Iri plus TRAIL-induced apoptosis and improved cell viability. Finally, combination of Iri and TRAIL inhibited tumor growth in the xenograft model. Collectively, our present study gave new insights into the effects of Iri on potentiating TRAIL-sensitivity, and suggested that Iri could be a potential candidate for sensitizer of TRAIL-resistant cancer cell treatment.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Proteínas Reguladoras de Apoptose/metabolismo
Apoptose/efeitos dos fármacos
Isoflavonas/administração & dosagem
Neoplasias Gástricas/tratamento farmacológico
Neoplasias Gástricas/metabolismo
Ligante Indutor de Apoptose Relacionado a TNF/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/administração & dosagem
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Sinergismo Farmacológico
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Masculino
Camundongos
Camundongos Nus
Neoplasias Gástricas/patologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Apoptosis Regulatory Proteins); 0 (Isoflavones); 0 (TNF-Related Apoptosis-Inducing Ligand); 6O4NX37350 (irigenin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


  4 / 5059 MEDLINE  
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[PMID]:29182023
[Au] Autor:Shi Q; Tao Z; Yang H; Fan Q; Wei D; Wan L; Lu X
[Ad] Endereço:a Key Lab of Transplant Engineering and Immunology , MOH, West China Hospital, Sichuan University , Chengdu , China.
[Ti] Título:PDGFRß-specific affibody-directed delivery of a photosensitizer, IR700, is efficient for vascular-targeted photodynamic therapy of colorectal cancer.
[So] Source:Drug Deliv;24(1):1818-1830, 2017 Nov.
[Is] ISSN:1521-0464
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Vascular-targeted photodynamic therapy (PDT) is an important strategy for cancer therapy. Conventional vascular-targeted PDT has been achieved by passive photosensitizer (PS) delivery, which involves a high risk of adverse effects. Active PS delivery is urgently required for vascular-targeted PDT. Although endothelial cells and pericytes are major cellular components of tumor blood vessels, little attention has been paid to pericyte-targeted PDT for cancer therapy. PDGFRß is abundantly expressed in the pericytes of various tumors. In this experiment, a dimeric Z affibody with a 0.9 nM affinity for PDGFRß was produced. The Z affibody showed PDGFRß-dependent pericyte binding. Intravenously injected Z affibody was predominantly distributed on pericytes and thus accumulated in LS174T tumor grafts. The conjugate of the Z affibody and IR700 dye, i.e. Z , bound to PDGFRß pericytes but not to PDGFRß LS174T tumor cells. Accordingly, Z -mediated PDT in vitro induced the death of pericytes but not of LS174T tumor cells. In mice bearing LS174T tumor grafts, Z -mediated PDT damaged tumor blood vessels, thus inducing tumor destruction by intensifying tissue hypoxia. The average mass of tumor grafts administered with Z -mediated PDT was approximately 20-30% of that of the control, indicating that pericyte-targeted PDT is efficient for cancer therapy. In addition, Z -mediated PDT increased the tumor uptake of TNF-related apoptosis-inducing ligand (TRAIL) injected post-illumination. Consequently, combination therapy of Z -mediated PDT and TRAIL showed greater tumor suppression than Z -mediated PDT- or TRAIL-based monotherapy. These results demonstrated that active vascular-targeted PDT could be achieved by using Z affibody-directed delivery of PS.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/administração & dosagem
Neoplasias Colorretais/tratamento farmacológico
Fármacos Fotossensibilizantes/administração & dosagem
Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular
Linhagem Celular Tumoral
Seres Humanos
Luz
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Pericitos/efeitos dos fármacos
Fotoquimioterapia/métodos
Ligante Indutor de Apoptose Relacionado a TNF/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Photosensitizing Agents); 0 (TNF-Related Apoptosis-Inducing Ligand); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1080/10717544.2017.1407011


  5 / 5059 MEDLINE  
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[PMID]:29172759
[Au] Autor:Wang S; Shao M; Zhong Z; Wang A; Cao J; Lu Y; Wang Y; Zhang J
[Ad] Endereço:a State Key Laboratory of Quality Research in Chinese Medicine , Institute of Chinese Medical Sciences, University of Macau , Macau , China.
[Ti] Título:Co-delivery of gambogic acid and TRAIL plasmid by hyaluronic acid grafted PEI-PLGA nanoparticles for the treatment of triple negative breast cancer.
[So] Source:Drug Deliv;24(1):1791-1800, 2017 Nov.
[Is] ISSN:1521-0464
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-based combination therapy and gene therapy are new strategies to potentially overcome the limitations of TRAIL, however, the lack of efficient and low toxic vectors remains the major obstacle. In this study, we developed a hyaluronic acid (HA)-decorated polyethylenimine-poly(d,l-lactide-co-glycolide) (PEI-PLGA) nanoparticle (NP) system for targeted co-delivery of TRAIL plasmid (pTRAIL) and gambogic acid (GA) in triple-negative breast cancer (TNBC) therapy. GA was encapsulated into the core of the PEI-PLGA NPs while pTRAIL was adsorbed onto the positive NP surface via charge adsorption. The coating of HA on PEI-PLGA NPs functions as a targeting ligand by binding to CD44 receptor of TNBC cells and a shell to neutralize the excess positive charge of inner NPs. The resultant pTRAIL and GA co-loaded HA-coated PEI-PLGA NPs exhibited spherical shape (121.5 nm) and could promote the internalization of loaded cargoes into TNBC cells through the CD44-dependent endocytic pathway. The dual drug-loaded NPs significantly augmented apoptotic cell death in vitro and inhibited TNBC tumor growth in vivo. This multifunctional NP system efficiently co-delivered GA and pTRAIL, thus representing a promising strategy to treat TNBC and bringing forth a platform strategy for co-delivery of therapeutic DNA and chemotherapeutic agents in combinatorial TNBC therapy.
[Mh] Termos MeSH primário: Ácido Hialurônico/administração & dosagem
Ácido Láctico/administração & dosagem
Nanopartículas/administração & dosagem
Plasmídeos/administração & dosagem
Polietilenoimina/administração & dosagem
Ácido Poliglicólico/administração & dosagem
Ligante Indutor de Apoptose Relacionado a TNF/administração & dosagem
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
Xantonas/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/administração & dosagem
Linhagem Celular Tumoral
Portadores de Fármacos/administração & dosagem
Seres Humanos
Receptores de Hialuronatos/metabolismo
Células MCF-7
Camundongos
Neoplasias de Mama Triplo Negativas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drug Carriers); 0 (Hyaluronan Receptors); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (Xanthones); 0 (polylactic acid-polyglycolic acid copolymer); 26009-03-0 (Polyglycolic Acid); 33X04XA5AT (Lactic Acid); 8N585K83U2 (gambogic acid); 9002-98-6 (Polyethyleneimine); 9004-61-9 (Hyaluronic Acid)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1080/10717544.2017.1406558


  6 / 5059 MEDLINE  
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[PMID]:29267342
[Au] Autor:Kuroki LM; Jin X; Dmitriev IP; Kashentseva EA; Powell MA; Mutch DG; Dietz AB; Curiel DT; Hawkins WG; Spitzer D
[Ad] Endereço:Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Washington University School of Medicine, St. Louis, MO, United States of America.
[Ti] Título:Adenovirus platform enhances transduction efficiency of human mesenchymal stem cells: An opportunity for cellular carriers of targeted TRAIL-based TR3 biologics in ovarian cancer.
[So] Source:PLoS One;12(12):e0190125, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Clinical application of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-based cancer therapeutics has not reached optimal potencies in part due to inadequate drug stability and inefficiencies in cancer-selective drug delivery. As such, innovative strategies regarding drug design and delivery are of utmost importance to achieve improved treatment results. With our current study, we aimed at exploring the groundwork for a two-stage targeting concept, which is based on the intrinsic tumor homing capacity of mesenchymal stem cells (MSCs) as cellular drug factories for the in situ production of our newly designed and biomarker-targeted TRAIL-based TR3 therapeutics. Since MSCs are primary cells, capable in vitro of only a limited number of cell divisions, identification of suitable strategies for their efficient genetic manipulation is of critical importance. We chose adenoviral (Ad) vectors as a transduction vehicle due to its ability to infect dividing and non-dividing cells and because of their limited restrictions regarding the packaging capacity of their genetic payload. In order to enhance the transduction efficacy of MSCs using Ad5 wild-type-based vectors, we tested a variety of fiber knob modifications on a panel of patient-derived MSC lines established from adipose tissue. We identified Ad5pK7, an Ad5 vector containing a polylysine fiber knob modification, exhibiting the highest transduction rates across a panel of 16 patient-derived MSC lines. We further demonstrated that MSCs could be efficiently transduced with an Ad5pK7 vector containing membrane-anchored and secreted TR3 expression units, including the MUC16 (CA125)-targeted variant Meso64-TR3. In both in vitro and in vivo experiments, MSC-derived Meso64-TR3 was far more potent on MUC16-expressing ovarian cancer compared to its non-targeted TR3 counterpart. Our findings thus provide the foundation to initiate further preclinical investigations on MSC-mediated treatment options in ovarian cancer using biomarker-targeted TR3-based biologics.
[Mh] Termos MeSH primário: Adenoviridae/genética
Produtos Biológicos/uso terapêutico
Células Mesenquimais Estromais/citologia
Neoplasias Ovarianas/terapia
Ligante Indutor de Apoptose Relacionado a TNF/uso terapêutico
Transdução Genética
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Neoplasias Ovarianas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Biological Products); 0 (TNF-Related Apoptosis-Inducing Ligand)
[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:171222
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190125


  7 / 5059 MEDLINE  
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[PMID]:28463038
[Au] Autor:Thabet NM; Moustafa EM
[Ad] Endereço:a Radiation Biology Department , National Centre for Radiation Research and Technology (NCRRT), Atomic Energy Authority , Cairo , Egypt.
[Ti] Título:Synergistic effect of Ebselen and gamma radiation on breast cancer cells.
[So] Source:Int J Radiat Biol;93(8):784-792, 2017 08.
[Is] ISSN:1362-3095
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To explore the synergistic effect of a seleno-organic compound Ebselen (Ebs) and/or γ-radiation to exert antitumor effects on human breast cancer (MCF-7) cell line in vitro. MATERIALS AND METHODS: Ebs cytotoxicity at various concentrations (10, 25, 50 and 75 µg), cell proliferation and clonogenic assay of Ebs and/or γ-radiation (at 1, 3 and 6 Gy), expression of p-IκBα and NF-κB, inflammatory cytokines levels (TNF-α, IL-2, INF-γ, IL-10 and TGF-ß), apoptotic factors (Caspase-3, Granzyme-B and TRAIL) and angiogenic factor (VEGF) were investigated. RESULTS: The results showed that the effective dosage of this combination was observed at 25 µg/ml of Ebs with γ-radiation at 6 Gy. Data displayed a significant reduction in NF-κB mRNA along with an elevation in granzyme-B mRNA and TRAIL mRNA expression. Furthermore, protein expression of caspase-3 was elevated, whereas p-IκBα and p-NF-κB(p65) protein expression was reduced significantly. Also, a significant decline in TNF-α, IL-2, INF-γ, TGF-ß with a significant increase in IL-10 levels were revealed. Meanwhile, a significant decrease in VEGF level and proliferation capacity were observed. CONCLUSIONS: We conclude that a combination of Ebs with radiotherapy has a major antitumor efficiency in inducing apoptosis and inhibiting cancer cell progression, due to the synergistic effect in regulating gene and protein expression, and in a modulating response of pro-and anti-inflammatory cytokines.
[Mh] Termos MeSH primário: Azóis/farmacologia
Neoplasias da Mama/patologia
Raios gama
Compostos Organosselênicos/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Apoptose/efeitos da radiação
Caspase 3/metabolismo
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/efeitos da radiação
Citocinas/metabolismo
Granzimas/metabolismo
Seres Humanos
Células MCF-7
NF-kappa B/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/efeitos da radiação
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Azoles); 0 (Cytokines); 0 (NF-kappa B); 0 (Organoselenium Compounds); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (Vascular Endothelial Growth Factor A); 40X2P7DPGH (ebselen); EC 3.4.21.- (Granzymes); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:IM; S
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1080/09553002.2017.1325024


  8 / 5059 MEDLINE  
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[PMID]:29187441
[Au] Autor:Pawlak A; DE Miguel D; Kutkowska J; Obminska-Mrukowicz B; Rapak A; Martinez-Lostao L
[Ad] Endereço:Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Wroclaw University of Environmental and Life Sciences, Wroclaw, Poland aleksandra.pawlak@upwr.edu.pl.
[Ti] Título:Flavopiridol Strongly Sensitizes Canine Lymphoma Cells to TRAIL-induced Apoptosis.
[So] Source:Anticancer Res;37(12):6655-6665, 2017 12.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Targeting the extrinsic apoptotic pathway is an interesting option for anticancer therapy. A protein which such ability is Apo2 ligand, also known as TNF-related apoptosis-inducing ligand (TRAIL). The aim of this study was to examine the possibility of sensitizing resistant CLBL-1 canine lymphoma cells to TRAIL-induced apoptosis by using flavopiridol (FVP) a cyclin-dependent kinase inhibitor (CDKs). MATERIALS AND METHODS: The CLBL-1 (canine B-cell lymphoma cell line) was used in the study. The effect of FVP and TRAIL treatment on apoptosis induction was assessed by flow cytometry and western blot. RESULTS: Although canine lymphoma cells were resistant to TRAIL-induced apoptosis, combination of this death ligand with FVP was able to overcome TRAIL resistance of CLBL-1 lymphoma cells. CONCLUSION: Our results demonstrated that although canine lymphoma cells were resistant to TRAIL-induced apoptosis, combination of this death ligand with FVP was able to overcome TRAIL resistance of CLBL-1 lymphoma cell line. Although further investigation is required to deepen the knowledge of TRAIL as an antitumor agent in canine cancers, our results open the door to future use of TRAIL-based treatment strategies in veterinary oncology.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Flavonoides/farmacologia
Piperidinas/farmacologia
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Western Blotting
Linhagem Celular Tumoral
Doenças do Cão/metabolismo
Doenças do Cão/patologia
Cães
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Sinergismo Farmacológico
Citometria de Fluxo
Seres Humanos
Linfoma/metabolismo
Linfoma/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Flavonoids); 0 (Piperidines); 0 (TNF-Related Apoptosis-Inducing Ligand); 45AD6X575G (alvocidib)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE


  9 / 5059 MEDLINE  
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[PMID]:29182622
[Au] Autor:Vondálová Blanárová O; Safaríková B; Herudková J; Krkoska M; Tománková S; Kahounová Z; Andera L; Bouchal J; Kharaishvili G; Král M; Sova P; Kozubík A; Hyrslová Vaculová A
[Ad] Endereço:Department of Cytokinetics, Institute of Biophysics, Czech Academy of Sciences, v.v.i., Brno, Czech Republic.
[Ti] Título:Cisplatin or LA-12 enhance killing effects of TRAIL in prostate cancer cells through Bid-dependent stimulation of mitochondrial apoptotic pathway but not caspase-10.
[So] Source:PLoS One;12(11):e0188584, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Searching for new strategies for effective elimination of human prostate cancer cells, we investigated the cooperative cytotoxic action of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and two platinum-based complexes, cisplatin or LA-12, and related molecular mechanisms. We demonstrated a notable ability of cisplatin or LA-12 to enhance the sensitivity of several human prostate cancer cell lines to TRAIL-induced cell death via an engagement of mitochondrial apoptotic pathway. This was accompanied by augmented Bid cleavage, Bak activation, loss of mitochondrial membrane potential, activation of caspase-8, -10, -9, and -3, and XIAP cleavage. RNAi-mediated silencing of Bid or Bak in Bax-deficient DU 145 cells suppressed the drug combination-induced cytotoxicity, further underscoring the involvement of mitochondrial signaling. The caspase-10 was dispensable for enhancement of cisplatin/LA-12 and TRAIL combination-induced cell death and stimulation of Bid cleavage. Importantly, we newly demonstrated LA-12-mediated enhancement of TRAIL-induced cell death in cancer cells derived from human patient prostate tumor specimens. Our results provide convincing evidence that employing TRAIL combined with cisplatin/LA-12 could contribute to more effective killing of prostate cancer cells compared to the individual action of the drugs, and offer new mechanistic insights into their cooperative anticancer action.
[Mh] Termos MeSH primário: Amantadina/análogos & derivados
Apoptose/efeitos dos fármacos
Proteína Agonista de Morte Celular de Domínio Interatuante com BH3/metabolismo
Caspase 10/metabolismo
Cisplatino/farmacologia
Mitocôndrias/efeitos dos fármacos
Compostos Organoplatínicos/farmacologia
Neoplasias da Próstata/patologia
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
[Mh] Termos MeSH secundário: Amantadina/farmacologia
Seres Humanos
Masculino
Mitocôndrias/metabolismo
Neoplasias da Próstata/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BH3 Interacting Domain Death Agonist Protein); 0 (BID protein, human); 0 (Organoplatinum Compounds); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (bis(acetato)(1-adamantylamine)amminedichloroplatinum(IV)); BF4C9Z1J53 (Amantadine); EC 3.4.22.- (Caspase 10); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188584


  10 / 5059 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



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