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Pesquisa : D03.633.100.127.125 [Categoria DeCS]
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[PMID]:28542306
[Au] Autor:Martínez M; Sorzano COS; Pascual-Montano A; Carazo JM
[Ad] Endereço:Biocomputing Unit, Nacional Center for Biotechnology (CSIC), Campus Universidad Autónoma de Madrid, Cantoblanco, Madrid, Spain.
[Ti] Título:Gene signature associated with benign neurofibroma transformation to malignant peripheral nerve sheath tumors.
[So] Source:PLoS One;12(5):e0178316, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Benign neurofibromas, the main phenotypic manifestations of the rare neurological disorder neurofibromatosis type 1, degenerate to malignant tumors associated to poor prognosis in about 10% of patients. Despite efforts in the field of (epi)genomics, the lack of prognostic biomarkers with which to predict disease evolution frustrates the adoption of appropriate early therapeutic measures. To identify potential biomarkers of malignant neurofibroma transformation, we integrated four human experimental studies and one for mouse, using a gene score-based meta-analysis method, from which we obtained a score-ranked signature of 579 genes. Genes with the highest absolute scores were classified as promising disease biomarkers. By grouping genes with similar neurofibromatosis-related profiles, we derived panels of potential biomarkers. The addition of promoter methylation data to gene profiles indicated a panel of genes probably silenced by hypermethylation. To identify possible therapeutic treatments, we used the gene signature to query drug expression databases. Trichostatin A and other histone deacetylase inhibitors, as well as cantharidin and tamoxifen, were retrieved as putative therapeutic means to reverse the aberrant regulation that drives to malignant cell proliferation and metastasis. This in silico prediction corroborated reported experimental results that suggested the inclusion of these compounds in clinical trials. This experimental validation supported the suitability of the meta-analysis method used to integrate several sources of public genomic information, and the reliability of the gene signature associated to the malignant evolution of neurofibromas to generate working hypotheses for prognostic and drug-responsive biomarkers or therapeutic measures, thus showing the potential of this in silico approach for biomarker discovery.
[Mh] Termos MeSH primário: Neoplasias da Bainha Neural/genética
Neurofibroma/genética
[Mh] Termos MeSH secundário: Animais
Biomarcadores Tumorais/genética
Cantaridina/farmacologia
Mapeamento Cromossômico
Simulação por Computador
Ilhas de CpG
Metilação de DNA
Ensaios de Seleção de Medicamentos Antitumorais
Inativação Gênica
Inibidores de Histona Desacetilases/farmacologia
Seres Humanos
Camundongos
Neoplasias da Bainha Neural/tratamento farmacológico
Neoplasias da Bainha Neural/patologia
Neurofibroma/tratamento farmacológico
Neurofibroma/patologia
Neurofibromatose 1/tratamento farmacológico
Neurofibromatose 1/genética
Neurofibromatose 1/patologia
Prognóstico
Regiões Promotoras Genéticas
Tamoxifeno/farmacologia
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Histone Deacetylase Inhibitors); 094ZI81Y45 (Tamoxifen); IGL471WQ8P (Cantharidin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178316


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[PMID]:28423415
[Au] Autor:Jiang M; Lü S; Zhang Y
[Ad] Endereço:Key Laboratory of Plant Protection Resources and Pest Management, National Ministry of Education, College of Plant Protection, Northwest A&F University, Yangling, Shaanxi 712100, China (mingjiang@nwsuaf.edu.cn; shuminlv@nwsuaf.edu.cn; yalinzh@nwsuaf.edu.cn).
[Ti] Título:The Potential Organ Involved in Cantharidin Biosynthesis in Epicauta chinensis Laporte (Coleoptera: Meloidae).
[So] Source:J Insect Sci;17(2), 2017 Jan 01.
[Is] ISSN:1536-2442
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cantharidin, a terpenoid defensive toxin mainly produced by blister beetles, is among the most widely known insect natural products in the world. However, little is known about the site of cantharidin biosynthesis in vivo. Our previous research showed that 3-hydroxy-3-methylglutary-CoA reductase (HMGR) is an essential enzyme in cantharidin biosynthesis. In this report, we further investigated cantharidin titer and HMGR mRNA expression levels in different tissues of male and female Epicauta chinensis, and performed a comparative analysis of HMGR transcript levels in male Tenebrio molitor, a Tenebrionidae beetle that cannot produce cantharidin. HMGR transcripts had a positive correlation with cantharidin production. Furthermore, the specifically high amounts of HMGR transcript and abundant cantharidin production in fat body of male E. chinensis indicated the process of cantharidin synthesis may occur in the fat body.
[Mh] Termos MeSH primário: Cantaridina/metabolismo
Coleópteros/genética
Corpo Adiposo/metabolismo
Hidroximetilglutaril-CoA Redutases/genética
Proteínas de Insetos/genética
Transcrição Genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Coleópteros/metabolismo
DNA Complementar/genética
DNA Complementar/metabolismo
Feminino
Hidroximetilglutaril-CoA Redutases/química
Hidroximetilglutaril-CoA Redutases/metabolismo
Proteínas de Insetos/química
Proteínas de Insetos/metabolismo
Masculino
Especificidade de Órgãos
Filogenia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Alinhamento de Sequência
Tenebrio/genética
Tenebrio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Insect Proteins); 0 (RNA, Messenger); EC 1.1.1.- (Hydroxymethylglutaryl CoA Reductases); IGL471WQ8P (Cantharidin)
[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:170420
[St] Status:MEDLINE
[do] DOI:10.1093/jisesa/iex021


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[PMID]:28274314
[Au] Autor:Liu Y; Li X; Zou Q; Liu L; Zhu X; Jia Q; Wang L; Yan R
[Ad] Endereço:Guizhou Provincial College-based Key Lab for Tumor Prevention and Treatment with Distinctive Medicines, Zunyi Medical University, Zunyi 563000, China.
[Ti] Título:[Inhibitory effect of magnesium cantharidate on human hepatoma SMMC-7721 cell proliferation by blocking MAPK signaling pathway].
[So] Source:Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi;33(3):347-351, 2017 Mar.
[Is] ISSN:1007-8738
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Objective To investigate the anticancer mechanism of magnesium cantharidate by observing its effect on the mitogen-activated protein kinase (MAPK) signaling pathway in human hepatoma SMMC-7721 cells. Methods The protein phosphatase 2A (PP2A) activity detection kit was used to detect the effects of magnesium cantharidate and okadaic acid (OA) on PP2A activity. After the treatment of SMMC-7721 cells with magnesium cantharidate and/or OA, mRNA levels of extracellular signal-regulated kinase 1 (ERK1), ERK2, p38MAPK, c-Jun N-terminal kinase 1 (JNK1) and JNK2 were detected by real-time quantitative PCR, and the protein expression levels and protein phosphorylation of ERK1, ERK2, p38 MAPK and JNK were determined by Western blotting. Results The effect of magnesium cantharidate on the activity of PP2A in SMMC-7721 cells was not evident at the concentration of 0.283 µmol/L, but the activity of PP2A was declined significantly at 0.567 µmol/L or higher concencentrations in a concentration-dependent manner. Likewise, OA also displayed apparent inhibitory effect on the activity of PP2A at 0.059 nmol/L. Compared with the control group, mRNA levels of ERK1 and ERK2 were not changed by magnesium cantharidate at 0.283 µmol/L, but they significantly declined at the concentrations greater than 0.567 µmol/L. In contrast, mRNA levels of ERK1 and ERK2 were significantly elevated by 0.059 nmol/L OA. mRNA levels of p38MAPK, JNK1 and JNK2 significantly increased after the treatment of 0.059 nmol/L OA or magnesium cantharidate at varying concentrations. Compared with the control group, phosphorylation levels of ERK1 and ERK2 were not changed by 0.283 µmol/L magnesium cantharidate, but decreased significantly when the concentration was 0.567 µmol/L or above. In contrast, the phosphorylation levels of ERK1 and ERK2 showed a significant increase in 0.059 nmol/L OA treated group. The phosphorylation levels of p38 MAPK, JNK1 and JNK2 were also significantly increased by 0.059 nmol/L OA or magnesium cantharidate in a concentration-dependent manner. Conclusion Magnesium cantharidate may inhibit the proliferation of SMMC-7721 cells by inhibiting the activity of PP2A and ERK1/2 signaling pathway.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Cantaridina/farmacologia
Carcinoma Hepatocelular/fisiopatologia
Proliferação Celular/efeitos dos fármacos
Neoplasias Hepáticas/fisiopatologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Magnésio/farmacologia
Inibidores de Proteínas Quinases/farmacologia
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/tratamento farmacológico
Carcinoma Hepatocelular/enzimologia
Linhagem Celular Tumoral
Seres Humanos
Neoplasias Hepáticas/tratamento farmacológico
Neoplasias Hepáticas/enzimologia
Proteína Fosfatase 2/antagonistas & inibidores
Proteína Fosfatase 2/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); EC 3.1.3.16 (Protein Phosphatase 2); I38ZP9992A (Magnesium); IGL471WQ8P (Cantharidin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE


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[PMID]:28167263
[Au] Autor:Liu X; Han M; Xu J; Geng S; Zhang Y; Ye X; Gou J; Yin T; He H; Tang X
[Ad] Endereço:Department of Pharmaceutics, College of Pharmacy, Shenyang Pharmaceutical University, Shenyang, Liaoning, PR China.
[Ti] Título:Asialoglycoprotein receptor-targeted liposomes loaded with a norcantharimide derivative for hepatocyte-selective targeting.
[So] Source:Int J Pharm;520(1-2):98-110, 2017 Mar 30.
[Is] ISSN:1873-3476
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In order to overcome the shortcomings associated with the clinical application of norcantharidin (NCTD), including intense irritation and a short half-life, and to obtain a hepatocyte-selective liposome system with high encapsulation efficiency (EE) and low leakage, we synthesized a C alkyl chain norcantharimide derivative of NCTD (2-tetradecylhexahydro-1H-4,7-epoxyisoindole-1,3(2H)-dione, N-14NCTDA). Asialoglycoprotein receptor-targeted, galactosylated liposomes loaded with N-14NCTDA (GAL-Lipo) were prepared by the lipid film hydration method. GAL-Lipo with a satisfactory particle size of approximately 120nm has a higher encapsulation efficiency of more than 98.0%, which is markedly increased compared with NCTD loaded liposomes (EE%=47.6%). In addition, GAL-Lipo remained stable for at least 1 month at 4°C. In cytotoxicity assays, GAL-Lipo demonstrated stronger cytotoxicity effects (IC =24.58µmolL ) on Hep G2 cells than free N-14NCTDA (100µmol/L) and conventional liposomes (Con-Lipo, 39.49µmol/L) without the GAL modification. GAL-Lipo can continuously accumulate in Hep G2 cells and be internalized into cells via two pathways, namely caveolin-dependent endocytosis and clathrin-dependent asialoglycoprotein receptors (ASGP-R) mediated endocytosis and produces considerably more significant cellular apoptosis. The results of vivo toxicity studies showed that GAL-Lipo dramatically reduced renal toxicity. In addition, GAL-Lipo has a markedly improved pharmacokinetic profile in vivo and a longer circulation time (AUC=6.700±2.964mgL h, t =1.347±0.519h) than Con-Lipo (AUC=2.319±0.121mgL h, t1/2z=0.413±0.238h). In conclusion, N-14NCTDA with an ideal logP is a better alternative for the treatment of primary hepatic carcinoma. GAL-Lipo offers an attractive strategy to specifically target hepatocytes via caveolin-dependent and clathrin-dependent asialoglycoprotein receptor-mediated endocytosis resulting in higher anticancer activity and fewer side-effects.
[Mh] Termos MeSH primário: Receptor de Asialoglicoproteína/metabolismo
Cantaridina/análogos & derivados
Sistemas de Liberação de Medicamentos
Hepatócitos/metabolismo
Lipossomos/farmacocinética
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Cantaridina/efeitos adversos
Cantaridina/síntese química
Cantaridina/química
Cantaridina/farmacocinética
Estabilidade de Medicamentos
Endocitose
Galactose/química
Células Hep G2
Hepatócitos/efeitos dos fármacos
Seres Humanos
Testes de Função Renal
Lipossomos/efeitos adversos
Lipossomos/química
Testes de Função Hepática
Masculino
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-tetradecylhexahydro-1H-4,7-epoxyisoindole-1,3(2H)-dione); 0 (Asialoglycoprotein Receptor); 0 (Liposomes); IGL471WQ8P (Cantharidin); X2RN3Q8DNE (Galactose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170208
[St] Status:MEDLINE


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[PMID]:28065690
[Au] Autor:Semenova G; Stepanova DS; Deyev SM; Chernoff J
[Ad] Endereço:Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, Russia; Cancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA, USA. Electronic address: Galina.Semenova@fccc.edu.
[Ti] Título:Medium throughput biochemical compound screening identifies novel agents for pharmacotherapy of neurofibromatosis type 1.
[So] Source:Biochimie;135:1-5, 2017 Apr.
[Is] ISSN:1638-6183
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The variable manifestation of phenotypes that occur in patients with neurofibromatosis type 1 (NF1) includes benign and malignant neurocutaneous tumors for which no adequate treatment exists. Cell-based screening of known bioactive compounds library identified the protein phosphatase 2A (PP2A) inhibitor Cantharidin and the L-type calcium channel blocker Nifedipine as potential candidates for NF1 pharmacotherapy. Validation of screening results using human NF1-associated malignant peripheral nerve sheath tumor (MPNST) cells showed that Cantharidin effectively impeded MPNST cell growth, while Nifedipine treatment significantly decreased local tumor growth in an MPNST xenograft animal model. These data suggest that inhibitors of PP2A, as well as calcium channel blockers, might be used in broader MPNST preclinical studies as single agents or in combinatorial therapeutic strategies.
[Mh] Termos MeSH primário: Cantaridina/uso terapêutico
Nifedipino/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/farmacologia
Cantaridina/efeitos adversos
Linhagem Celular
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Feminino
Fibroblastos/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Camundongos
Camundongos Nus
Neoplasias da Bainha Neural/tratamento farmacológico
Neurofibromatose 1
Nifedipino/efeitos adversos
Proteína Fosfatase 2/antagonistas & inibidores
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); EC 3.1.3.16 (Protein Phosphatase 2); I9ZF7L6G2L (Nifedipine); IGL471WQ8P (Cantharidin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170110
[St] Status:MEDLINE


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[PMID]:27893465
[Au] Autor:Rathod KS; Kapil V; Velmurugan S; Khambata RS; Siddique U; Khan S; Van Eijl S; Gee LC; Bansal J; Pitrola K; Shaw C; D'Acquisto F; Colas RA; Marelli-Berg F; Dalli J; Ahluwalia A
[Ti] Título:Accelerated resolution of inflammation underlies sex differences in inflammatory responses in humans.
[So] Source:J Clin Invest;127(1):169-182, 2017 Jan 03.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cardiovascular disease occurs at lower incidence in premenopausal females compared with age-matched males. This variation may be linked to sex differences in inflammation. We prospectively investigated whether inflammation and components of the inflammatory response are altered in females compared with males. METHODS: We performed 2 clinical studies in healthy volunteers. In 12 men and 12 women, we assessed systemic inflammatory markers and vascular function using brachial artery flow-mediated dilation (FMD). In a further 8 volunteers of each sex, we assessed FMD response to glyceryl trinitrate (GTN) at baseline and at 8 hours and 32 hours after typhoid vaccine. In a separate study in 16 men and 16 women, we measured inflammatory exudate mediators and cellular recruitment in cantharidin-induced skin blisters at 24 and 72 hours. RESULTS: Typhoid vaccine induced mild systemic inflammation at 8 hours, reflected by increased white cell count in both sexes. Although neutrophil numbers at baseline and 8 hours were greater in females, the neutrophils were less activated. Systemic inflammation caused a decrease in FMD in males, but an increase in females, at 8 hours. In contrast, GTN response was not altered in either sex after vaccine. At 24 hours, cantharidin formed blisters of similar volume in both sexes; however, at 72 hours, blisters had only resolved in females. Monocyte and leukocyte counts were reduced, and the activation state of all major leukocytes was lower, in blisters of females. This was associated with enhanced levels of the resolving lipids, particularly D-resolvin. CONCLUSIONS: Our findings suggest that female sex protects against systemic inflammation-induced endothelial dysfunction. This effect is likely due to accelerated resolution of inflammation compared with males, specifically via neutrophils, mediated by an elevation of the D-resolvin pathway. TRIAL REGISTRATION: ClinicalTrials.gov NCT01582321 and NRES: City Road and Hampstead Ethics Committee: 11/LO/2038. FUNDING: The authors were funded by multiple sources, including the National Institute for Health Research, the British Heart Foundation, and the European Research Council.
[Mh] Termos MeSH primário: Mediadores da Inflamação/sangue
Nitroglicerina/administração & dosagem
Caracteres Sexuais
Vacinas Tíficas-Paratíficas/administração & dosagem
[Mh] Termos MeSH secundário: Adolescente
Adulto
Vesícula/sangue
Vesícula/induzido quimicamente
Artéria Braquial/fisiopatologia
Cantaridina/administração & dosagem
Cantaridina/efeitos adversos
Feminino
Seres Humanos
Inflamação/sangue
Inflamação/induzido quimicamente
Contagem de Leucócitos
Masculino
Meia-Idade
Fatores de Tempo
Vasodilatação/efeitos dos fármacos
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inflammation Mediators); 0 (Typhoid-Paratyphoid Vaccines); G59M7S0WS3 (Nitroglycerin); IGL471WQ8P (Cantharidin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161129
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE


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[PMID]:27591962
[Au] Autor:Yang X; Tong J; Guo L; Qian Z; Chen Q; Qi R; Qiu Y
[Ad] Endereço:Department of Neurosurgery, South Campus, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
[Ti] Título:Bundling potent natural toxin cantharidin within platinum (IV) prodrugs for liposome drug delivery and effective malignant neuroblastoma treatment.
[So] Source:Nanomedicine;13(1):287-296, 2017 Jan.
[Is] ISSN:1549-9642
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuroblastoma (NB) is one of the most commonly seen malignancies in childhood and infancy. Cantharidin is a highly potent natural toxin that possesses potent anti-tumor properties on various cancers including NB. However, exposure to cantharidin can cause severe chemical burns and application of cantharidin for cancer therapy is limited. Here we report a strategy of bundling cantharidin within a hybrid platinum (IV) prodrug conjugate. This hydrophobic drug conjugate, ie, CanPt can be further formulated into liposome for drug delivery to minimize the exposure of cantharidin to normal cells for efficient chemotherapeutic agent against NB.
[Mh] Termos MeSH primário: Cantaridina/administração & dosagem
Portadores de Fármacos/química
Lipossomos/química
Neuroblastoma/tratamento farmacológico
Platina/administração & dosagem
Pró-Fármacos/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Liberação Controlada de Fármacos
Ensaios de Seleção de Medicamentos Antitumorais
Feminino
Camundongos
Camundongos Endogâmicos BALB C
Nanoconjugados/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Carriers); 0 (Liposomes); 0 (Nanoconjugates); 0 (Prodrugs); 49DFR088MY (Platinum); IGL471WQ8P (Cantharidin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160905
[St] Status:MEDLINE


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[PMID]:27113412
[Au] Autor:Li CC; Yu FS; Fan MJ; Chen YY; Lien JC; Chou YC; Lu HF; Tang NY; Peng SF; Huang WW; Chung JG
[Ad] Endereço:Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, 404.
[Ti] Título:Anticancer effects of cantharidin in A431 human skin cancer (Epidermoid carcinoma) cells in vitro and in vivo.
[So] Source:Environ Toxicol;32(3):723-738, 2017 Mar.
[Is] ISSN:1522-7278
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cantharidin (CTD), a potential anticancer agent of Traditional Chinese Medicine has cytotxic effects in different human cancer cell lines. The cytotoxic effects of CTD on A431 human skin cancer (epidermoid carcinoma) cells in vitro and in A431 cell xenograft mouse model were examined. In vitro, A431 human skin cell were treated with CTD for 24 and 48 h. Cell phase distribution, ROS production, Ca release, Caspase activity and the level of apoptosis associated proteins were measured. In vivo, A431 cell xenograft mouse model were examined. CTD-induced cell morphological changes and decreased percentage of viable A431 cells via G0/G1 phase arrest and induced apoptosis. CTD-induced G0/G1 phase arrest through the reduction of protein levels of cyclin E, CDK6, and cyclin D in A431 cells. CTD-induced cell apoptosis of A431 cells also was confirm by DNA gel electrophoresis showed CTD-induced DNA fragmentation. CTD reduced the mitochondrial membrane potential and stimulated release of cytochrome c, AIF and Endo G in A431 cells. Flow cytometry demonstrated that CTD increased activity of caspase-8, -9 and -3. However, when cells were pretreated with specific caspase inhibitors activity was reduced and cell viability increased. CTD increased protein levels of death receptors such as DR4, DR5, TRAIL and levels of the active form of caspase-8, -9 and -3 in A431 cells. AIF and Endo G proteins levels were also enhanced by CTD. In vivo studies showed that CTD significantly inhibited A431 cell xenograft tumors in mice. Taken together, these in vitro and in vivo results provide insight into the mechanisms of CTD on cell growth and tumor production. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 723-738, 2017.
[Mh] Termos MeSH primário: Antineoplásicos/toxicidade
Apoptose/efeitos dos fármacos
Cantaridina/toxicidade
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/uso terapêutico
Cantaridina/uso terapêutico
Carcinoma de Células Escamosas/tratamento farmacológico
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/patologia
Caspases/genética
Caspases/metabolismo
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Ciclina D/metabolismo
Citocromos c/metabolismo
Fragmentação do DNA/efeitos dos fármacos
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Seres Humanos
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Espécies Reativas de Oxigênio/metabolismo
Receptores de Morte Celular/metabolismo
Transdução de Sinais/efeitos dos fármacos
Neoplasias Cutâneas/tratamento farmacológico
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/patologia
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Transplante Heterólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cyclin D); 0 (Reactive Oxygen Species); 0 (Receptors, Death Domain); 0 (TNF-Related Apoptosis-Inducing Ligand); 9007-43-6 (Cytochromes c); EC 3.4.22.- (Caspases); IGL471WQ8P (Cantharidin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170322
[Lr] Data última revisão:
170322
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160427
[St] Status:MEDLINE
[do] DOI:10.1002/tox.22273


  9 / 593 MEDLINE  
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[PMID]:27989101
[Au] Autor:Sun X; Cai X; Yang J; Chen J; Guo C; Cao P
[Ad] Endereço:Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210028, China.
[Ti] Título:Cantharidin Overcomes Imatinib Resistance by Depleting BCR-ABL in Chronic Myeloid Leukemia.
[So] Source:Mol Cells;39(12):869-876, 2016 12.
[Is] ISSN:0219-1032
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Cantharidin (CTD) is an active compound isolated from the traditional Chinese medicine blister beetle and displayed anticancer properties against various types of cancer cells. However, little is known about its effect on human chronic myeloid leukemia (CML) cells, including imatinib-resistant CML cells. The objective of this study was to investigate whether CTD could overcome imatinib resistance in imatinib-resistant CML cells and to explore the possible underlying mechanisms associated with the effect. Our results showed that CTD strongly inhibited the growth of both imatinib-sensitive and imatinib-resistant CML cells. CTD induced cell cycle arrest at mitotic phase and triggered DNA damage in CML cells. The ATM/ATR inhibitor CGK733 abrogated CTD-induced mitotic arrest but promoted the cytotoxic effects of CTD. In addition, we demonstrated that CTD downregulated the expression of the BCR-ABL protein and suppressed its downstream signal transduction. Real-time quantitative PCR revealed that CTD inhibited BCR-ABL at transcriptional level. Knockdown of BCR-ABL increased the cell-killing effects of CTD in K562 cells. These findings indicated that CTD overcomes imatinib resistance through depletion of BCR-ABL. Taken together, CTD is an important new candidate agent for CML therapy.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Cantaridina/farmacologia
Proteínas de Fusão bcr-abl/deficiência
Mesilato de Imatinib/farmacologia
Leucemia Mielogênica Crônica BCR-ABL Positiva/tratamento farmacológico
[Mh] Termos MeSH secundário: Cantaridina/administração & dosagem
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Dano ao DNA
Sinergismo Farmacológico
Proteínas de Fusão bcr-abl/genética
Proteínas de Fusão bcr-abl/metabolismo
Técnicas de Silenciamento de Genes
Seres Humanos
Mesilato de Imatinib/administração & dosagem
Células K562
Leucemia Mielogênica Crônica BCR-ABL Positiva/genética
Leucemia Mielogênica Crônica BCR-ABL Positiva/metabolismo
Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
8A1O1M485B (Imatinib Mesylate); EC 2.7.10.2 (Fusion Proteins, bcr-abl); IGL471WQ8P (Cantharidin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161219
[St] Status:MEDLINE
[do] DOI:10.14348/molcells.2016.0023


  10 / 593 MEDLINE  
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[PMID]:27930712
[Au] Autor:Su CC; Lee KI; Chen MK; Kuo CY; Tang CH; Liu SH
[Ad] Endereço:Graduate Institute of Basic Medical Science, College of Medicine, China Medical University, Taichung, Taiwan.
[Ti] Título:Cantharidin Induced Oral Squamous Cell Carcinoma Cell Apoptosis via the JNK-Regulated Mitochondria and Endoplasmic Reticulum Stress-Related Signaling Pathways.
[So] Source:PLoS One;11(12):e0168095, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oral cancer is a subtype of head and neck cancer which represents 2.65% of all human malignancies. Most of oral cancer is histopathologically diagnosed as oral squamous cell carcinoma (OSCC). OSCC is characterized by a high degree of local invasion and a high rate of metastasis to the cervical lymph nodes. How to prevention and treatment of OSCC is important and imperative. Here, we investigated the therapeutic effect and molecular mechanism of cantharidin, an active compound isolated from blister beetles, on OSCC in vitro. Results showed that cantharidin significantly decreased cell viability in human tongue squamous carcinoma-derived SAS, CAL-27, and SCC-4 cell lines. The further mechanistic studies were carried out in SAS cells. Cantharidin also significantly increased apoptosis-related signals, including caspase-9, caspase-7 and caspase-3 proteins. Besides, cantharidin decreased mitochondrial transmembrane potential (MMP) and induced cytochrome c and apoptosis inducing factor (AIF) release. Cantharidin also increased Bax, Bid, and Bak protein expressions and decreased Bcl-2 protein expression. Cantharidin could also increase the endoplasmic reticulum (ER) stress signals, including the expressions of phosphorylated eIF-2α and CHOP, but not Grp78 and Grp94. Furthermore, cantharidin reduced pro-caspase-12 protein expression. In signals of mitogen-activated protein kinases, cantharidin increased the phosphorylation of JNK, but not ERK and p38. Transfection of shRNA-JNK to OSCC cells effectively reversed the cantharidin-induced cell apoptotic signals, including the mitochondrial and ER stress-related signaling molecules. Taken together, these findings suggest that cantharidin induces apoptosis in OSCC cells via the JNK-regulated mitochondria and ER stress-related signaling pathways.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Apoptose/efeitos dos fármacos
Cantaridina/uso terapêutico
Carcinoma de Células Escamosas/tratamento farmacológico
Retículo Endoplasmático/fisiologia
Sistema de Sinalização das MAP Quinases/fisiologia
Neoplasias Bucais/tratamento farmacológico
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Apoptose/fisiologia
Western Blotting
Carcinoma de Células Escamosas/fisiopatologia
Linhagem Celular Tumoral
Seres Humanos
Técnicas In Vitro
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/fisiologia
Neoplasias Bucais/fisiopatologia
Reação em Cadeia da Polimerase em Tempo Real
Neoplasias da Língua/tratamento farmacológico
Neoplasias da Língua/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); IGL471WQ8P (Cantharidin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161209
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0168095



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