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[PMID]:26902406
[Au] Autor:Durmaz I; Guven EB; Ersahin T; Ozturk M; Calis I; Cetin-Atalay R
[Ad] Endereço:Department of Molecular Biology and Genetics, Faculty of Science, Bilkent University, Ankara, Turkey. Electronic address: durmaz@bilkent.edu.tr.
[Ti] Título:Liver cancer cells are sensitive to Lanatoside C induced cell death independent of their PTEN status.
[So] Source:Phytomedicine;23(1):42-51, 2016 Jan 15.
[Is] ISSN:1618-095X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hepatocellular carcinoma is the second deadliest cancer with limited treatment options. Loss of PTEN causes the P13K/Akt pathway to be hyperactive which contributes to cell survival and resistance to therapeutics in various cancers, including the liver cancer. Hence molecules targeting this pathway present good therapeutic strategies for liver cancer. HYPOTHESIS: It was previously reported that Cardiac glycosides possessed antitumor activity by inducing apoptosis of multiple cancer cells through oxidative stress. However, whether Cardiac glycoside Lanatoside C can induce oxidative stress in liver cancer cells and induce cell death both in vitro and in vivo remains unknown. METHODS: Cell viability was measured by SRB assay. Cell death analysis was investigated by propidium iodide staining with flow cytometry and PARP cleavage. DCFH-DA staining and cytometry were used for intracellular ROS measurement. Protein levels were analyzed by western blot analysis. Antitumor activity was investigated on mice xenografts in vivo. RESULTS: In this study, we found that Cardiac glycosides, particularly Lanatoside C from Digitalis ferruginea could significantly inhibit PTEN protein adequate Huh7 and PTEN deficient Mahlavu human liver cancer cell proliferation by the induction of apoptosis and G2/M arrest in the cells. Lanatoside C was further shown to induce oxidative stress and alter ERK and Akt pathways. Consequently, JNK1 activation resulted in extrinsic apoptotic pathway stimulation in both cells while JNK2 activation involved in the inhibition of cell survival only in PTEN deficient cells. Furthermore, nude mice xenografts followed by MRI showed that Lanatoside C caused a significant decrease in the tumor size. In this study apoptosis induction by Lanatoside C was characterized through ROS altered ERK and Akt pathways in both PTEN adequate epithelial and deficient mesenchymal liver cancer cells. CONCLUSION: The results indicated that Lanatoside C could be contemplated in liver cancer therapeutics, particularly in PTEN deficient tumors. This is due to Lanatoside C's stress inducing action on ERK and Akt pathways through differential activation of JNK1 and JNK2 by GSK3ß.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Carcinoma Hepatocelular/patologia
Lanatosídeos/farmacologia
Neoplasias Hepáticas/patologia
PTEN Fosfo-Hidrolase/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Proliferação Celular
Digitalis/química
Seres Humanos
Camundongos
Camundongos Nus
Estresse Oxidativo
Transdução de Sinais
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lanatosides); 5RR3JFZ771 (lanatoside C); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160224
[St] Status:MEDLINE


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[PMID]:26821916
[Au] Autor:Shi H; Mao X; Zhong Y; Liu Y; Zhao X; Yu K; Zhu R; Wei Y; Zhu J; Sun H; Mao Y; Zeng Q
[Ad] Endereço:The Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
[Ti] Título:Lanatoside C Promotes Foam Cell Formation and Atherosclerosis.
[So] Source:Sci Rep;6:20154, 2016 Jan 29.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Lanatoside C's impact on atherosclerosis is poorly understood. The present study was conducted to determine whether lanatoside C affects the development of atherosclerosis in apolipoprotein E-deficient (ApoE(-/-)) mice. ApoE(-/-) mice were administered either phosphate-buffered saline (PBS) containing 0.1% DMSO (the vehicle control group) or lanatoside C at low (1 mg/kg per day) or high (2 mg/kg per day) doses, and fed a Western diet for 12 weeks. Lanatoside C dose-dependently aggravated the development of atherosclerosis in the ApoE(-/-) mice compared with the vehicle control group. In an effort to determine the mechanism by which lanatoside C increased atherosclerosis, we found that lanatoside C significantly promoted the uptake of oxidised low-density lipoprotein (oxLDL) and increased foam-cell formation by upregulation of scavenger receptor class A (SR-A) and the class B scavenger receptor (CD36) in macrophages. Meanwhile, the effects of lanatoside C were abolished using small interfering RNA (siRNA) inhibition of peroxisome proliferator-activated receptors ß/δ (PPARß/δ). Overall, our data demonstrate that lanatoside C aggravates the development of atherosclerosis by inducing PPARß/δ expression, which mediates upregulation of SR-A and CD36, and promotes oxLDL uptake and foam-cell formation.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Células Espumosas/metabolismo
Lanatosídeos/toxicidade
Macrófagos Peritoneais/metabolismo
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas E/deficiência
Aterosclerose/induzido quimicamente
Aterosclerose/genética
Aterosclerose/patologia
Dieta Ocidental/efeitos adversos
Células Espumosas/patologia
Macrófagos Peritoneais/patologia
Masculino
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Lanatosides); 5RR3JFZ771 (lanatoside C)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170113
[Lr] Data última revisão:
170113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160130
[St] Status:MEDLINE
[do] DOI:10.1038/srep20154


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[PMID]:26756216
[Au] Autor:Kang MA; Kim MS; Kim W; Um JH; Shin YJ; Song JY; Jeong JH
[Ad] Endereço:Research Center for Radiotherapy, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
[Ti] Título:Lanatoside C suppressed colorectal cancer cell growth by inducing mitochondrial dysfunction and increased radiation sensitivity by impairing DNA damage repair.
[So] Source:Oncotarget;7(5):6074-87, 2016 Feb 02.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiac glycosides are clinically used for cardiac arrhythmias. In this study, we investigated the mechanism responsible for anti-cancer and radiosensitizing effects of lanatoside C in colorectal cancer cells. Lanatoside C-treated cells showed classic patterns of autophagy, which may have been caused by lanatoside C-induced mitochondrial aggregation or degeneration. This mitochondrial dysfunction was due to disruption of K+ homeostasis, possibly through inhibition of Na+/K+-ATPase activity. In addition, lanatoside C sensitized HCT116 cells (but not HT-29 cells) to radiation in vitro. γ-H2AX, a representative marker of DNA damage, were sustained longer after combination of irradiation with lanatoside C, suggesting lanatoside C impaired DNA damage repair processes. Recruitment of 53BP1 to damaged DNA, a critical initiation step for DNA damage repair signaling, was significantly suppressed in lanatoside C-treated HCT116 cells. This may have been due to defects in the RNF8- and RNF168-dependent degradation of KDM4A/JMJD2A that increases 53BP1 recruitment to DNA damage sites. Although lanatoside C alone reduced tumor growth in the mouse xenograft tumor model, combination of lanatoside C and radiation inhibited tumor growth more than single treatments. Thus, lanatoside C could be a potential molecule for anti-cancer drugs and radiosensitizing agents.
[Mh] Termos MeSH primário: Neoplasias Colorretais/tratamento farmacológico
Reparo do DNA/efeitos dos fármacos
Lanatosídeos/farmacologia
Mitocôndrias/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Autofagia/efeitos dos fármacos
Processos de Crescimento Celular/efeitos dos fármacos
Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Dano ao DNA
Células HCT116
Células HT29
Seres Humanos
Camundongos
Mitocôndrias/genética
Tolerância a Radiação/efeitos dos fármacos
Radiossensibilizantes/farmacologia
Distribuição Aleatória
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lanatosides); 0 (Radiation-Sensitizing Agents); 5RR3JFZ771 (lanatoside C)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160113
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.6832


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[PMID]:26708508
[Au] Autor:Crommentuijn MH; Maguire CA; Niers JM; Vandertop WP; Badr CE; Würdinger T; Tannous BA
[Ad] Endereço:Experimental Therapeutics and Molecular Imaging Laboratory, Neuroscience Center, Department of Neurology, Massachusetts General Hospital, Boston, MA, USA; Program in Neuroscience, Harvard Medical School, Boston, MA, USA; Neuro-oncology Research Group, Cancer Center Amsterdam, Department of Neurosurg
[Ti] Título:Intracranial AAV-sTRAIL combined with lanatoside C prolongs survival in an orthotopic xenograft mouse model of invasive glioblastoma.
[So] Source:Mol Oncol;10(4):625-34, 2016 Apr.
[Is] ISSN:1878-0261
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma (GBM) is the most common malignant brain tumor in adults. We designed an adeno-associated virus (AAV) vector for intracranial delivery of secreted, soluble tumor necrosis factor-related apoptosis-inducing ligand (sTRAIL) to GBM tumors in mice and combined it with the TRAIL-sensitizing cardiac glycoside, lanatoside C (lan C). We applied this combined therapy to two different GBM models using human U87 glioma cells and primary patient-derived GBM neural spheres in culture and in orthotopic GBM xenograft models in mice. In U87 cells, conditioned medium from AAV2-sTRAIL expressing cells combined with lan C induced 80% cell death. Similarly, lan C sensitized primary GBM spheres to sTRAIL causing over 90% cell death. In mice bearing intracranial U87 tumors treated with AAVrh.8-sTRAIL, administration of lan C caused a decrease in tumor-associated Fluc signal, while tumor size increased within days of stopping the treatment. Another round of lan C treatment re-sensitized GBM tumor to sTRAIL-induced cell death. AAVrh.8-sTRAIL treatment alone and combined with lanatoside C resulted in a significant decrease in tumor growth and longer survival of mice bearing orthotopic invasive GBM brain tumors. In summary, AAV-sTRAIL combined with lanatoside C induced cell death in U87 glioma cells and patient-derived GBM neural spheres in culture and in vivo leading to an increased in overall mice survival.
[Mh] Termos MeSH primário: Neoplasias Encefálicas
Dependovirus
Vetores Genéticos
Glioblastoma
Lanatosídeos/farmacologia
Neoplasias Experimentais
Ligante Indutor de Apoptose Relacionado a TNF
[Mh] Termos MeSH secundário: Animais
Neoplasias Encefálicas/genética
Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/patologia
Neoplasias Encefálicas/terapia
Linhagem Celular Tumoral
Glioblastoma/genética
Glioblastoma/metabolismo
Glioblastoma/patologia
Glioblastoma/terapia
Xenoenxertos
Seres Humanos
Camundongos
Camundongos Nus
Invasividade Neoplásica
Transplante de Neoplasias
Neoplasias Experimentais/genética
Neoplasias Experimentais/metabolismo
Neoplasias Experimentais/patologia
Neoplasias Experimentais/terapia
Ligante Indutor de Apoptose Relacionado a TNF/biossíntese
Ligante Indutor de Apoptose Relacionado a TNF/genética
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lanatosides); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFSF10 protein, human); H4BU39831E (lanatoside A)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151229
[St] Status:MEDLINE


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[PMID]:26083423
[Au] Autor:Wang W; Liu H; Yang J; Shen Y
[Ad] Endereço:The First People's Hospital of Kunshan Kunshan, Jiangsu, China.
[Ti] Título:Acute Pulmonary Edema After Cranioplasty.
[So] Source:J Neurosurg Anesthesiol;28(1):84, 2016 Jan.
[Is] ISSN:1537-1921
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Complicações Pós-Operatórias/terapia
Edema Pulmonar/terapia
Crânio/cirurgia
Retalhos Cirúrgicos
[Mh] Termos MeSH secundário: Acidentes de Trânsito
Doença Aguda
Anti-Inflamatórios/uso terapêutico
Craniectomia Descompressiva
Diuréticos/uso terapêutico
Feminino
Furosemida/uso terapêutico
Seres Humanos
Lanatosídeos/uso terapêutico
Metilprednisolona/uso terapêutico
Oxigênio/uso terapêutico
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Diuretics); 0 (Lanatosides); 5RR3JFZ771 (lanatoside C); 7LXU5N7ZO5 (Furosemide); S88TT14065 (Oxygen); X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160401
[Lr] Data última revisão:
160401
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150618
[St] Status:MEDLINE
[do] DOI:10.1097/ANA.0000000000000197


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[PMID]:25251726
[Au] Autor:Cheung YY; Chen KC; Chen H; Seng EK; Chu JJ
[Ad] Endereço:Laboratory of Molecular RNA Virology and Antiviral Strategies, Department of Microbiology, Yong Loo Lin School of Medicine, National University Health System, 5 Science Drive 2, National University of Singapore, Singapore 117597, Singapore.
[Ti] Título:Antiviral activity of lanatoside C against dengue virus infection.
[So] Source:Antiviral Res;111:93-9, 2014 Nov.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Dengue infection poses a serious threat globally due to its recent rapid spread and rise in incidence. Currently, there is no approved vaccine or effective antiviral drug for dengue virus infection. In response to the urgent need for the development of an effective antiviral for dengue virus, the US Drug Collection library was screened in this study to identify compounds with anti-dengue activities. Lanatoside C, an FDA approved cardiac glycoside was identified as a candidate anti-dengue compound. Our data revealed that lanatoside C has an IC50 of 0.19µM for dengue virus infection in HuH-7 cells. Dose-dependent reduction in dengue viral RNA and viral proteins synthesis were also observed upon treatment with increasing concentrations of lanatoside C. Time of addition study indicated that lanatoside C inhibits the early processes of the dengue virus replication cycle. Furthermore, lanatoside C can effectively inhibit all four serotypes of dengue virus, flavivirus Kunjin, alphavirus Chikungunya and Sindbis virus as well as the human enterovirus 71. These findings suggest that lanatoside C possesses broad spectrum antiviral activity against several groups of positive-sense RNA viruses.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Vírus da Dengue/efeitos dos fármacos
Dengue/virologia
Lanatosídeos/farmacologia
[Mh] Termos MeSH secundário: Dengue/tratamento farmacológico
Vírus da Dengue/genética
Vírus da Dengue/fisiologia
Avaliação Pré-Clínica de Medicamentos
Seres Humanos
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Lanatosides); 5RR3JFZ771 (lanatoside C)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:141202
[Lr] Data última revisão:
141202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140925
[St] Status:MEDLINE


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[PMID]:24801379
[Au] Autor:Teng J; Hejazi S; Badr CE; Tannous BA
[Ad] Endereço:Experimental Therapeutics and Molecular Imaging Laboratory, Neuroscience Center, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA; Program in Neuroscience, Harvard Medical School, Boston, Massachusetts, USA.
[Ti] Título:Systemic anticancer neural stem cells in combination with a cardiac glycoside for glioblastoma therapy.
[So] Source:Stem Cells;32(8):2021-32, 2014 Aug.
[Is] ISSN:1549-4918
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor-tropic properties of neural stem cells (NSCs) have been shown to serve as a novel strategy to deliver therapeutic genes to tumors. Recently, we have reported that the cardiac glycoside lanatoside C (Lan C) sensitizes glioma cells to the anticancer agent tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Here, we engineered an FDA-approved human NSC line to synthesize and secrete TRAIL and the Gaussia luciferase (Gluc) blood reporter. We showed that upon systemic injection, these cells selectively migrate toward tumors in the mice brain across the blood-brain barrier, target invasive glioma stem-like cells, and induce tumor regression when combined with Lan C. Gluc blood assay revealed that 30% of NSCs survived 1 day postsystemic injection and around 0.5% of these cells remained viable after 5 weeks in glioma-bearing mice. This study demonstrates the potential of systemic injection of NSCs to deliver anticancer agents, such as TRAIL, which yields glioma regression when combined with Lan C.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/patologia
Terapia Genética/métodos
Glioblastoma/patologia
Células-Tronco Neurais/transplante
Ligante Indutor de Apoptose Relacionado a TNF/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Glicosídeos Cardíacos/farmacologia
Linhagem Celular Tumoral
Movimento Celular/fisiologia
Técnicas de Cocultura
Modelos Animais de Doenças
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Lanatosídeos/farmacologia
Camundongos
Camundongos Nus
Ligante Indutor de Apoptose Relacionado a TNF/genética
Transfecção
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Cardiac Glycosides); 0 (Lanatosides); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFSF10 protein, human); 5RR3JFZ771 (lanatoside C)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140508
[St] Status:MEDLINE
[do] DOI:10.1002/stem.1727


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[PMID]:24241792
[Au] Autor:Bao H; Wang J; Zhou D; Han Z; Su L; Zhang Y; Ye X; Xu C; Wang Y; Li Q
[Ad] Endereço:Department of Respiratory Medicine, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, No. 2800 Gongwei Road, Huinan Town, Shanghai, 201399, China.
[Ti] Título:Protein-protein interaction network analysis in chronic obstructive pulmonary disease.
[So] Source:Lung;192(1):87-93, 2014 Feb.
[Is] ISSN:1432-1750
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The aim of this study was to investigate the gene expression profile of chronic obstructive pulmonary disease (COPD) patients and non-COPD patients. METHODS: Microarray raw data (GSE29133) was downloaded from Gene Expression Omnibus, including three COPD samples and three normal controls. Gene expression profiling was performed using Affymetrix human genome u133 plus 2.0 GeneChip. Differentially expressed genes were identified by Student's t test and genes with p < 0.05 were considered significantly changed. Up- and downregulated genes were submitted to the molecular signatures database (MSigDB) to search for a possible association with other previously published gene expression signatures. Furthermore, we constructed a COPD protein-protein interaction (PPI) network and used the connectivity map (cMap) to query for potential drugs for COPD. RESULTS: A total of 680 upregulated genes and 530 downregulated genes in COPD were identified. The MSigDB investigation found that upregulated genes were highly similar to gene signatures that respond to interferon and downregulated genes were similar to erythroid progenitor cells from fetal livers of E13.5 embryos with KLF1 knocked out. A PPI network consisting of 814 gene/proteins and 2,613 interactions was identified by Search Tool for the Retrieval of Interacting Genes. The cMap predicted helveticoside, disulfiram, and lanatoside C as the top three possible drugs that could perhaps treat COPD. CONCLUSION: Comprehensive analysis of the gene expression profile for COPD versus control reveals helveticoside, disulfiram, and lanatoside C as potential molecular targets in COPD. This evidence provides a new breakthrough in the medical treatment of patients with COPD.
[Mh] Termos MeSH primário: Mapeamento de Interação de Proteínas
Mapas de Interação de Proteínas
Proteínas/metabolismo
Doença Pulmonar Obstrutiva Crônica/metabolismo
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Mineração de Dados
Bases de Dados Genéticas
Glicosídeos Digitálicos/uso terapêutico
Dissulfiram/uso terapêutico
Desenho de Drogas
Perfilação da Expressão Gênica/métodos
Regulação da Expressão Gênica
Predisposição Genética para Doença
Seres Humanos
Lanatosídeos/uso terapêutico
Terapia de Alvo Molecular
Análise de Sequência com Séries de Oligonucleotídeos
Fenótipo
Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico
Doença Pulmonar Obstrutiva Crônica/genética
Estrofantinas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RETRACTED PUBLICATION
[Nm] Nome de substância:
0 (Digitalis Glycosides); 0 (Lanatosides); 0 (Proteins); 0 (Strophanthins); 52OAE3C457 (helveticoside); 5RR3JFZ771 (lanatoside C); TR3MLJ1UAI (Disulfiram)
[Em] Mês de entrada:1409
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131119
[St] Status:MEDLINE
[do] DOI:10.1007/s00408-013-9509-x


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[PMID]:22870937
[Au] Autor:Ueda Y; Mishiro K; Yoshida K; Furuta T; Kawabata T
[Ad] Endereço:Institute for Chemical Research, Kyoto University, Uji, Kyoto 611-0011, Japan.
[Ti] Título:Regioselective diversification of a cardiac glycoside, lanatoside C, by organocatalysis.
[So] Source:J Org Chem;77(18):7850-7, 2012 Sep 21.
[Is] ISSN:1520-6904
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acylation of lanatoside C in the presence of organocatalyst 5 gave the C(4'''')-O-acylate in up to 90% regioselectivity (catalyst-controlled regioselectivity). Various functionalized acyl groups can be introduced at the C(4'''')-OH by a mixed anhydride method in the presence of 5 or the related organocatalyst. On the other hand, DMAP-catalyzed acylation of lanatoside C gave the C(3'''')-O-acylate in up to 97% regioselectivity (substrate-controlled regioselectivity). Thus, diverse regioselective introduction of acyl groups among eight free hydroxy groups of lanatoside C was achieved.
[Mh] Termos MeSH primário: Glicosídeos Cardíacos/química
Lanatosídeos/química
Lanatosídeos/síntese química
[Mh] Termos MeSH secundário: Acilação
Catálise
Estereoisomerismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cardiac Glycosides); 0 (Lanatosides); 5RR3JFZ771 (lanatoside C)
[Em] Mês de entrada:1304
[Cu] Atualização por classe:120921
[Lr] Data última revisão:
120921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120809
[St] Status:MEDLINE


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[PMID]:21757445
[Au] Autor:Badr CE; Wurdinger T; Nilsson J; Niers JM; Whalen M; Degterev A; Tannous BA
[Ad] Endereço:Neuroscience Center and Molecular Neurogenetics Unit, Department of Neurology, Massachusetts General Hospital, Boston, MA, USA.
[Ti] Título:Lanatoside C sensitizes glioblastoma cells to tumor necrosis factor-related apoptosis-inducing ligand and induces an alternative cell death pathway.
[So] Source:Neuro Oncol;13(11):1213-24, 2011 Nov.
[Is] ISSN:1523-5866
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human glioblastoma (GBM) cells are notorious for their resistance to apoptosis-inducing therapeutics. We have identified lanatoside C as a sensitizer of GBM cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced cell death partly by upregulation of the death receptor 5. We show that lanatoside C sensitizes GBM cells to TRAIL-induced apoptosis in a GBM xenograft model in vivo. Lanatoside C on its own serves as a therapeutic agent against GBM by activating a caspase-independent cell death pathway. Cells treated with lanatoside C showed necrotic cell morphology with absence of caspase activation, low mitochondrial membrane potential, and early intracellular ATP depletion. In conclusion, lanatoside C sensitizes GBM cells to TRAIL-induced cell death and mitigates apoptosis resistance of glioblastoma cells by inducing an alternative cell death pathway. To our knowledge, this is one of the first examples of use of caspase-independent cell death inducers to trigger tumor regression in vivo. Activation of such mechanism may be a useful strategy to counter resistance of cancer cells to apoptosis.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos
Glioblastoma/tratamento farmacológico
Glioblastoma/patologia
Lanatosídeos/uso terapêutico
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
[Mh] Termos MeSH secundário: Animais
Autofagia/efeitos dos fármacos
Western Blotting
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/patologia
Caspases/metabolismo
Morte Celular
Células Cultivadas
Glioblastoma/metabolismo
Seres Humanos
Camundongos
Camundongos Nus
Necrose
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/genética
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lanatosides); 0 (RNA, Messenger); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (TNF-Related Apoptosis-Inducing Ligand); 5RR3JFZ771 (lanatoside C); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1202
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110716
[St] Status:MEDLINE
[do] DOI:10.1093/neuonc/nor067



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