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[PMID]:28524232
[Au] Autor:Stelling AL; Xu Y; Zhou H; Choi SH; Clay MC; Merriman DK; Al-Hashimi HM
[Ad] Endereço:Department of Biochemistry, Duke University Medical Center, Durham, NC, USA.
[Ti] Título:Robust IR-based detection of stable and fractionally populated G-C and A-T Hoogsteen base pairs in duplex DNA.
[So] Source:FEBS Lett;591(12):1770-1784, 2017 Jun.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Noncanonical G-C and A-T Hoogsteen base pairs can form in duplex DNA and play roles in recognition, damage repair, and replication. Identifying Hoogsteen base pairs in DNA duplexes remains challenging due to difficulties in resolving syn versus antipurine bases with X-ray crystallography; and size limitations and line broadening can make them difficult to characterize by NMR spectroscopy. Here, we show how infrared (IR) spectroscopy can identify G-C and A-T Hoogsteen base pairs in duplex DNA across a range of different structural contexts. The utility of IR-based detection of Hoogsteen base pairs is demonstrated by characterizing the first example of adjacent A-T and G-C Hoogsteen base pairs in a DNA duplex where severe broadening complicates detection with NMR.
[Mh] Termos MeSH primário: Pareamento de Bases
DNA/química
Modelos Moleculares
[Mh] Termos MeSH secundário: Adenina/análogos & derivados
Adenina/química
Adenina/metabolismo
Antibacterianos/química
Antibacterianos/metabolismo
Antibacterianos/farmacologia
Pareamento de Bases/efeitos dos fármacos
Sítios de Ligação
Instabilidade Cromossômica/efeitos dos fármacos
Dicroísmo Circular
DNA/metabolismo
Equinomicina/química
Equinomicina/metabolismo
Equinomicina/farmacologia
Estudos de Viabilidade
Guanina/análogos & derivados
Guanina/química
Guanina/metabolismo
Ligações de Hidrogênio/efeitos dos fármacos
Concentração de Íons de Hidrogênio
Ressonância Magnética Nuclear Biomolecular
Conformação de Ácido Nucleico/efeitos dos fármacos
Espectrofotometria
Espectrofotometria Infravermelho
Espectroscopia de Infravermelho com Transformada de Fourier
Estereoisomerismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 1ATY0M8242 (1-methylguanine); 512-64-1 (Echinomycin); 5142-22-3 (1-methyladenine); 5Z93L87A1R (Guanine); 9007-49-2 (DNA); JAC85A2161 (Adenine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12681


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[PMID]:28183349
[Au] Autor:Yao Y; Wang L; Zhou J; Zhang X
[Ad] Endereço:MDCL-4084, Department of Pathology & Molecular Medicine, McMaster University, 1280 Main Street West, Hamilton, ON, L8S4K1, Canada. yaoy15@mcmaster.ca.
[Ti] Título:HIF-1α inhibitor echinomycin reduces acute graft-versus-host disease and preserves graft-versus-leukemia effect.
[So] Source:J Transl Med;15(1):28, 2017 Feb 10.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute graft-versus-host disease (aGVHD) remains a major obstacle against favorable clinical outcomes following allogeneic hematopoietic stem cell transplantation (allo-HSCT). T helper cells including Th17 play key roles in aGVHD pathogenesis. Donor regulatory T cell (Tregs) adoptive therapy reduces aGVHD without weakening graft-versus-leukemia effect (GVL) in both mouse and human, although the purification and ex vivo expansion of Tregs in clinical scenarios remain costly and technically demanding. Hypoxia-inducible factor 1 alpha (HIF-1α) is a key molecule switch that attenuates Treg but promotes Th17 development. However, whether pharmacological inhibition of HIF-1α reduces aGVHD via increasing Treg development and diminishing Th17 responses remains unexplored. METHODS: By using alloantigen-specific mixed lymphocyte culture and murine models of aGVHD and GVL, we evaluated the impacts of HIF-1α inhibition by echinomycin on the alloantigen-specific CD4 T cell responses ex vivo, as well as on aGVHD and GVL effect following allo-HSCT. RESULTS: Ex vivo echinomycin treatment resulted in increased number of Tregs in the culture as well as reduced alloantigen-specific Th17 and Th1 responses. In vivo echinomycin treatment reduced GVHD scores and prolonged survival of mice following allo-HSCT, which is associated with increased number of donor Tregs and reduced number of Th17 and Th1 in lymphoid tissues. In murine model of leukemia, echinomycin treatment preserved GVL effect and prolonged leukemia free survival following allo-HSCT. CONCLUSIONS: Echinomycin treatment reduces aGVHD and preserves GVL effect via increasing donor Treg development and diminishing alloantigen-specific Th17 and Th1 responses following allo-HSCT, presumably via direct inhibition of HIF-1α that results in preferential Treg differentiation during alloantigen-specific CD4 T cell responses. These findings highlight pharmacological inhibition of HIF-1α as a promising strategy in GVHD prophylaxis.
[Mh] Termos MeSH primário: Equinomicina/uso terapêutico
Doença Enxerto-Hospedeiro/tratamento farmacológico
Efeito Enxerto vs Leucemia/efeitos dos fármacos
Subunidade alfa do Fator 1 Induzível por Hipóxia/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Intervalo Livre de Doença
Equinomicina/farmacologia
Feminino
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Isoantígenos/imunologia
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Linfócitos T Auxiliares-Indutores/efeitos dos fármacos
Linfócitos T Auxiliares-Indutores/imunologia
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Células Th17/efeitos dos fármacos
Células Th17/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Isoantigens); 512-64-1 (Echinomycin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170211
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1132-9


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[PMID]:28179306
[Au] Autor:Lim YS; Cha W; Park MW; Jeong WJ; Ahn SH
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Ilsan Hospital, Dongguk University, Goyang, Republic of Korea.
[Ti] Título:HIF1α in Tumorigenesis of Adenoid Cystic Carcinoma.
[So] Source:Anticancer Res;37(2):599-606, 2017 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Tumor hypoxia induces hypoxia-inducible factor-1α (HIF1α), which can influence tumorigenesis and metastasis. We evaluated the expression of HIF1α and the effect of HIF1α inhibitors in adenoid cystic carcinoma (ACC). MATERIALS AND METHODS: HIF1α expression was demonstrated in ACC cell lines (ACC2 and ACCM). The effect of HIF1α inhibitors was evaluated. A systemic metastasis model was developed. The number of metastatic pulmonary nodules were analyzed. RESULTS: The ACCM cell line demonstrated greater HIF1α expression and invasion than ACC2. The expression of HIF1α and invasion of ACC cells were blocked by HIF1α siRNA. HIF1α inhibitors 17-N-allylamino-17-demethoxygeldanamycin (17AAG) and echinomycin inhibited cell invasion. 17AAG inhibited metastasis in the animal model, although not statistically significantly. CONCLUSION: HIF1α siRNA and 17AAG and echinomycin blocked invasion by ACC2 and ACCM cells. 17AAG exhibited therapeutic potential for inhibition of metastasis. Our results provide positive evidence that HIF1α is a promising research pathway for therapy of ACC.
[Mh] Termos MeSH primário: Carcinoma Adenoide Cístico/genética
Transformação Celular Neoplásica/genética
Regulação Neoplásica da Expressão Gênica/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
[Mh] Termos MeSH secundário: Animais
Benzoquinonas/farmacologia
Western Blotting
Carcinoma Adenoide Cístico/tratamento farmacológico
Carcinoma Adenoide Cístico/patologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/genética
Transformação Celular Neoplásica/metabolismo
Equinomicina/farmacologia
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/antagonistas & inibidores
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Lactamas Macrocíclicas/farmacologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/prevenção & controle
Neoplasias Pulmonares/secundário
Camundongos Endogâmicos BALB C
Camundongos Nus
Interferência de RNA
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzoquinones); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Lactams, Macrocyclic); 4GY0AVT3L4 (tanespimycin); 512-64-1 (Echinomycin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170227
[Lr] Data última revisão:
170227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170210
[St] Status:MEDLINE


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[PMID]:28126820
[Au] Autor:Camunas-Soler J; Alemany A; Ritort F
[Ad] Endereço:Small Biosystems Lab, Departament de Física de la Matèria Condensada, Facultat de Física, Universitat de Barcelona, Barcelona, Spain.
[Ti] Título:Experimental measurement of binding energy, selectivity, and allostery using fluctuation theorems.
[So] Source:Science;355(6323):412-415, 2017 01 27.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thermodynamic bulk measurements of binding reactions rely on the validity of the law of mass action and the assumption of a dilute solution. Yet, important biological systems such as allosteric ligand-receptor binding, macromolecular crowding, or misfolded molecules may not follow these assumptions and may require a particular reaction model. Here we introduce a fluctuation theorem for ligand binding and an experimental approach using single-molecule force spectroscopy to determine binding energies, selectivity, and allostery of nucleic acids and peptides in a model-independent fashion. A similar approach could be used for proteins. This work extends the use of fluctuation theorems beyond unimolecular folding reactions, bridging the thermodynamics of small systems and the basic laws of chemical equilibrium.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/química
Ligantes
Termodinâmica
[Mh] Termos MeSH secundário: Regulação Alostérica
Sítios de Ligação
Desoxirribonuclease EcoRI/química
Equinomicina/química
Ligação Proteica
Imagem Individual de Molécula
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Ligands); 512-64-1 (Echinomycin); EC 3.1.21.- (Deoxyribonuclease EcoRI)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170128
[St] Status:MEDLINE
[do] DOI:10.1126/science.aah4077


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[PMID]:27840375
[Au] Autor:Fadhillah; Yoshioka S; Nishimura R; Yamamoto Y; Kimura K; Okuda K
[Ad] Endereço:Laboratory of Reproductive Physiology, Graduate School of Environmental and Life Sciences, Okayama University, Okayama 700-8530, Japan.
[Ti] Título:Hypoxia-inducible factor 1 mediates hypoxia-enhanced synthesis of progesterone during luteinization of granulosa cells.
[So] Source:J Reprod Dev;63(1):75-85, 2017 Feb 16.
[Is] ISSN:1348-4400
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Hypoxia has been suggested to enhance progesterone (P4) synthesis in luteinizing granulosa cells (GCs), but the mechanism is unclear. The present study was designed to test the hypothesis that the hypoxia-induced increase in P4 synthesis during luteinization in bovine GCs is mediated by hypoxia-inducible factor 1 (HIF-1). GCs obtained from small antral follicles were cultured with 2 µg/ml insulin in combination with 10 µM forskolin for 24 h as a model of luteinizing GCs. To examine the influence of HIF-1 on P4 synthesis, we determined the effect of changes in protein expression of the α-subunit of HIF-1 (HIF1A) on P4 production and on the expression levels of StAR, P450scc, and 3ß-HSD. CoCl (100 µM), a hypoxia-mimicking chemical, increased HIF-1α protein expression in luteinizing GCs. After the upregulation of HIF-1α, we observed an increase in P4 production and in the gene and protein expression levels of StAR in CoCl -treated luteinizing GCs. In contrast, CoCl did not affect the expression of either P450scc or 3ß-HSD. Echinomycin, a small-molecule inhibitor of HIF-1's DNA-binding activity, attenuated the effects of CoCl and of low oxygen tension (10% O ) on P4 production and StAR expression in luteinizing GCs. Overall, these findings suggest that HIF-1 is one of the factors that upregulate P4 in GCs during luteinization.
[Mh] Termos MeSH primário: Células da Granulosa/citologia
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Luteinização/efeitos dos fármacos
Progesterona/biossíntese
[Mh] Termos MeSH secundário: Animais
Bovinos
Sobrevivência Celular
Colforsina/metabolismo
DNA/química
DNA Complementar/metabolismo
Equinomicina/química
Feminino
Células da Granulosa/metabolismo
Hipóxia
Hormônio Luteinizante/metabolismo
Folículo Ovariano/metabolismo
Ovário/metabolismo
Oxigênio/metabolismo
RNA Mensageiro/metabolismo
Ativação Transcricional
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (RNA, Messenger); 1F7A44V6OU (Colforsin); 4G7DS2Q64Y (Progesterone); 512-64-1 (Echinomycin); 9002-67-9 (Luteinizing Hormone); 9007-49-2 (DNA); S88TT14065 (Oxygen)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161115
[St] Status:MEDLINE
[do] DOI:10.1262/jrd.2016-068


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[PMID]:26673007
[Au] Autor:Ponnurangam S; Dandawate PR; Dhar A; Tawfik OW; Parab RR; Mishra PD; Ranadive P; Sharma R; Mahajan G; Umar S; Weir SJ; Sugumar A; Jensen RA; Padhye SB; Balakrishnan A; Anant S; Subramaniam D
[Ad] Endereço:Department of Molecular and Integrative Physiology, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
[Ti] Título:Quinomycin A targets Notch signaling pathway in pancreatic cancer stem cells.
[So] Source:Oncotarget;7(3):3217-32, 2016 Jan 19.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer stem cells (CSCs) appear to explain many aspects of the neoplastic evolution of tumors and likely account for enhanced therapeutic resistance following treatment. Dysregulated Notch signaling, which affects CSCs plays an important role in pancreatic cancer progression. We have determined the ability of Quinomycin to inhibit CSCs and the Notch signaling pathway. Quinomycin treatment resulted in significant inhibition of proliferation and colony formation in pancreatic cancer cell lines, but not in normal pancreatic epithelial cells. Moreover, Quinomycin affected pancreatosphere formation. The compound also decreased the expression of CSC marker proteins DCLK1, CD44, CD24 and EPCAM. In addition, flow cytometry studies demonstrated that Quinomycin reduced the number of DCLK1+ cells. Furthermore, levels of Notch 1-4 receptors, their ligands Jagged1, Jagged2, DLL1, DLL3, DLL4 and the downstream target protein Hes-1 were reduced. The γ-secretase complex proteins, Presenilin 1, Nicastrin, Pen2, and APH-1, required for Notch activation also exhibited decreased expression. Ectopic expression of the Notch Intracellular Domain (NICD) partially rescued the cells from Quinomycin mediated growth suppression. To determine the effect of Quinomycin on tumor growth in vivo, nude mice carrying tumor xenografts were administered Quinomycin intraperitoneally every day for 21 days. Treatment with the compound significantly inhibited tumor xenograft growth, coupled with significant reduction in the expression of CSC markers and Notch signaling proteins. Together, these data suggest that Quinomycin is a potent inhibitor of pancreatic cancer that targets the stem cells by inhibiting Notch signaling proteins.
[Mh] Termos MeSH primário: Antibióticos Antineoplásicos/farmacologia
Equinomicina/farmacologia
Neoplasias Pancreáticas/tratamento farmacológico
Receptores Notch/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Secretases da Proteína Precursora do Amiloide/antagonistas & inibidores
Animais
Apoptose/efeitos dos fármacos
Antígeno CD24/metabolismo
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Progressão da Doença
Resistência a Medicamentos Antineoplásicos
Molécula de Adesão da Célula Epitelial/metabolismo
Citometria de Fluxo
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Seres Humanos
Receptores de Hialuronatos/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Masculino
Camundongos
Camundongos Nus
Transplante de Neoplasias
Células-Tronco Neoplásicas
Pâncreas/patologia
Neoplasias Pancreáticas/patologia
Proteínas Serina-Treonina Quinases/metabolismo
Receptores Notch/metabolismo
Transplante Heterólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 0 (CD24 Antigen); 0 (CD24 protein, human); 0 (CD44 protein, human); 0 (EPCAM protein, human); 0 (Epithelial Cell Adhesion Molecule); 0 (Hyaluronan Receptors); 0 (Intracellular Signaling Peptides and Proteins); 0 (Receptors, Notch); 512-64-1 (Echinomycin); EC 2.7.1.11 (DCLK1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.4.- (Amyloid Precursor Protein Secretases)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151218
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.6560


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[PMID]:26654708
[Au] Autor:Tsuzuki T; Okada H; Shindoh H; Shimoi K; Nishigaki A; Kanzaki H
[Ad] Endereço:a Department of Obstetrics and Gynecology , Kansai Medical University , Osaka , Japan.
[Ti] Título:Effects of the hypoxia-inducible factor-1 inhibitor echinomycin on vascular endothelial growth factor production and apoptosis in human ectopic endometriotic stromal cells.
[So] Source:Gynecol Endocrinol;32(4):323-8, 2016.
[Is] ISSN:1473-0766
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recent evidence points to a possible role for hypoxia-inducible factor (HIF)-1 in the pathogenesis and development of endometriosis. The objectives of this study were to investigate the critical role of HIF-1 in endometriosis and the effect of the HIF-1 inhibitor echinomycin on human ectopic endometriotic stromal cells (eESCs). Ectopic endometriotic tissues were obtained from 20 patients, who received an operation for ovarian endometriomas. We examined vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1 (SDF-1) production, HIF-1 expression, cell proliferation and apoptosis of eESCs. Cobalt chloride (CoCl2) significantly induced expression of HIF-1α protein and VEGF production in a time-dependent manner in eESCs, but reduced SDF-1 production. VEGF production was significantly suppressed by treatment of 100 nM echinomycin without causing cell toxicity, but 0.1-10 nM echinomycin or 100 nM progestin had no significant effect. SDF-1 production was not affected by echinomycin treatment at any dose. Echinomycin inhibited cell proliferation and induced apoptotic cell death of the eESCs, and significantly inhibited expression of the anti-apoptotic proteins Bcl-2 and Bcl-xL. Echinomycin inhibits VEGF production and induces apoptosis of eESCs by suppression of Bcl-2 and Bcl-xL. These findings suggest the unique therapeutic potential for echinomycin as an inhibitor of HIF-1 activation for endometriosis treatment.
[Mh] Termos MeSH primário: Equinomicina/uso terapêutico
Endometriose/tratamento farmacológico
Endométrio/efeitos dos fármacos
Fator 1 Induzível por Hipóxia/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adulto
Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Quimiocina CXCL12/metabolismo
Coristoma/tratamento farmacológico
Avaliação Pré-Clínica de Medicamentos
Equinomicina/farmacologia
Endométrio/metabolismo
Feminino
Seres Humanos
Meia-Idade
Células Estromais/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CXCL12 protein, human); 0 (Chemokine CXCL12); 0 (Hypoxia-Inducible Factor 1); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 512-64-1 (Echinomycin)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170111
[Lr] Data última revisão:
170111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151215
[St] Status:MEDLINE
[do] DOI:10.3109/09513590.2015.1121225


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[PMID]:26593927
[Au] Autor:Zhen X; Gong T; Liu F; Zhang PC; Zhou WQ; Li Y; Zhu P
[Ad] Endereço:State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, 1 Xian Nong Tan Street, Xicheng District, Beijing 100050, China. zhenxin@imm.ac.cn.
[Ti] Título:A New Analogue of Echinomycin and a New Cyclic Dipeptide from a Marine-Derived Streptomyces sp. LS298.
[So] Source:Mar Drugs;13(11):6947-61, 2015 Nov 18.
[Is] ISSN:1660-3397
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Quinomycin G (1), a new analogue of echinomycin, together with a new cyclic dipeptide, cyclo-(l-Pro-4-OH-l-Leu) (2), as well as three known antibiotic compounds tirandamycin A (3), tirandamycin B (4) and staurosporine (5), were isolated from Streptomyces sp. LS298 obtained from a marine sponge Gelliodes carnosa. The planar and absolute configurations of compounds 1 and 2 were established by MS, NMR spectral data analysis and Marfey's method. Furthermore, the differences in NMR data of keto-enol tautomers in tirandamycins were discussed for the first time. Antibacterial and anti-tumor activities of compound 1 were measured against 15 drug-sensitive/resistant strains and 12 tumor cell lines. Compound 1 exhibited moderate antibacterial activities against Staphylococcuse pidermidis, S. aureus, Enterococcus faecium, and E. faecalis with the minimum inhibitory concentration (MIC) values ranged from 16 to 64 µg/mL. Moreover, it displayed remarkable anti-tumor activities; the highest activity was observed against the Jurkat cell line (human T-cell leukemia) with an IC50 value of 0.414 µM.
[Mh] Termos MeSH primário: Dipeptídeos/farmacologia
Equinomicina/análogos & derivados
Streptomyces/metabolismo
[Mh] Termos MeSH secundário: Animais
Antibacterianos/administração & dosagem
Antibacterianos/isolamento & purificação
Antibacterianos/farmacologia
Antineoplásicos/administração & dosagem
Antineoplásicos/isolamento & purificação
Antineoplásicos/farmacologia
Bactérias/efeitos dos fármacos
Linhagem Celular Tumoral
Dipeptídeos/administração & dosagem
Dipeptídeos/isolamento & purificação
Farmacorresistência Bacteriana
Equinomicina/administração & dosagem
Equinomicina/isolamento & purificação
Equinomicina/farmacologia
Seres Humanos
Concentração Inibidora 50
Células Jurkat
Espectroscopia de Ressonância Magnética
Espectrometria de Massas
Testes de Sensibilidade Microbiana
Poríferos/microbiologia
Streptomyces/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Antineoplastic Agents); 0 (Dipeptides); 11113-76-1 (quinomycin); 512-64-1 (Echinomycin)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151214
[Lr] Data última revisão:
151214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151124
[St] Status:MEDLINE
[do] DOI:10.3390/md13116947


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[PMID]:26050843
[Au] Autor:Kambayashi S; Igase M; Kobayashi K; Kimura A; Shimokawa Miyama T; Baba K; Noguchi S; Mizuno T; Okuda M
[Ad] Endereço:Laboratory of Veterinary Internal Medicine, The United Graduate School of Veterinary Science, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan.
[Ti] Título:Hypoxia inducible factor 1α expression and effects of its inhibitors in canine lymphoma.
[So] Source:J Vet Med Sci;77(11):1405-12, 2015 Nov.
[Is] ISSN:1347-7439
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Hypoxic conditions in various cancers are believed to relate with their malignancy, and hypoxia inducible factor-1α (HIF-1α) has been shown to be a major regulator of the response to low oxygen. In this study, we examined HIF-1α expression in canine lymphoma using cell lines and clinical samples and found that these cells expressed HIF-1α. Moreover, the HIF-1α inhibitors, echinomycin, YC-1 and 2-methoxyestradiol, suppressed the proliferation of canine lymphoma cell lines. In a xenograft model using NOD/scid mice, echinomycin treatment resulted in a dose-dependent regression of the tumor. Our results suggest that HIF-1α contributes to the proliferation and/or survival of canine lymphoma cells. Therefore, HIF-1α inhibitors may be potential agents to treat canine lymphoma.
[Mh] Termos MeSH primário: Equinomicina/farmacologia
Subunidade alfa do Fator 1 Induzível por Hipóxia/antagonistas & inibidores
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Linfoma/veterinária
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Doenças do Cão
Cães
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Linfoma/metabolismo
Camundongos
Neoplasias Experimentais/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hypoxia-Inducible Factor 1, alpha Subunit); 512-64-1 (Echinomycin)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:161018
[Lr] Data última revisão:
161018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150609
[St] Status:MEDLINE
[do] DOI:10.1292/jvms.15-0258


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[PMID]:25980053
[Au] Autor:Watanabe K
[Ti] Título:[Effective use of heterologous hosts for characterization of biosynthetic enzymes allows production of natural products and promotes new natural product discovery].
[So] Source:Jpn J Antibiot;68(1):55-67, 2015 Feb.
[Is] ISSN:0368-2781
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Mh] Termos MeSH primário: Antibacterianos/biossíntese
Produtos Biológicos/metabolismo
Descoberta de Drogas
[Mh] Termos MeSH secundário: Distinções e Prêmios
Equinomicina/biossíntese
Piperazinas/metabolismo
Compostos de Espiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Biological Products); 0 (Piperazines); 0 (Spiro Compounds); 0 (spirotryprostatin A); 512-64-1 (Echinomycin)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:161116
[Lr] Data última revisão:
161116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150519
[St] Status:MEDLINE



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