Base de dados : MEDLINE
Pesquisa : G04.146 [Categoria DeCS]
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  1 / 39730 MEDLINE  
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[PMID]:29408405
[Au] Autor:Wang H; Park BS; Lim WA; Ki JS
[Ad] Endereço:Department of Biotechnology, Sangmyung University, Seoul 03016, South Korea.
[Ti] Título:CpMCA, a novel metacaspase gene from the harmful dinoflagellate Cochlodinium polykrikoides and its expression during cell death.
[So] Source:Gene;651:70-78, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Metacaspases (MCAs) are cysteine proteases that share sequence homology with caspases, and may play roles in programmed cell death (PCD). In the present study, we identified a novel MCA gene (CpMCA) from the red tide dinoflagellate Cochlodinium polykrikoides, and examined its molecular characteristics and gene expression in response to algicide-induced cell death. CpMCA cDNA is 1164 bp in length, containing a dinoflagellate spliced leader sequence (dinoSL), an 879-bp open reading frame (ORF), which codes for a 293-aa protein, and a poly (A) tail. Multi-sequence comparison indicated that CpMCA belongs to type I MCA, but it has a different structure at the N-terminal. Phylogenetic analysis showed that C. polykrikoides may have acquired the MCA gene from bacteria by means of horizontal gene transfer (HGT). In addition, expressions of CpMCA significantly increased following exposure to the common algicides copper sulfate and oxidizing chlorine, which trigger cell death in dinoflagellates, suggesting that CpMCA may be involved in cell death.
[Mh] Termos MeSH primário: Caspases/genética
Dinoflagelados/genética
[Mh] Termos MeSH secundário: Morte Celular/efeitos dos fármacos
Morte Celular/genética
DNA Complementar
DNA de Protozoário
Dinoflagelados/efeitos dos fármacos
Dinoflagelados/enzimologia
Expressão Gênica
Transferência Genética Horizontal
Genes Bacterianos
Genes de Protozoários
Herbicidas/farmacologia
Filogenia
Análise de Sequência de DNA
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (DNA, Protozoan); 0 (Herbicides); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  2 / 39730 MEDLINE  
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[PMID]:29408396
[Au] Autor:Wang W; Zhang H; Wei X; Yang L; Yang B; Zhang L; Li J; Jiang YQ
[Ad] Endereço:State Key Laboratory of Crop Stress Biology for Arid Areas, College of Life Sciences, Northwest A & F University, Yangling, Shaanxi 712100, China.
[Ti] Título:Functional characterization of calcium-dependent protein kinase (CPK) 2 gene from oilseed rape (Brassica napus L.) in regulating reactive oxygen species signaling and cell death control.
[So] Source:Gene;651:49-56, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Calcium-dependent protein kinases (CPKs), being Ser/Thr protein kinases found only in plants and some protozoans are calcium sensors that regulate diverse biological processes. However, the function and mode of CPKs in oilseed rape (Brassica napus) remain elusive. In this study, we identified CPK2 from oilseed rape as a novel regulator of reactive oxygen species (ROS) and cell death. BnaCPK2 was identified to be located at the endoplasmic reticulum membrane. Expression of BnaCPK2 was induced during Bax-induced cell death. Overexpression of the constitutively active form of BnaCPK2 led to significantly more accumulation of ROS and cell death than the full-length CPK2, which is supported by various measurements of physiological data. In addition, a quantitative RT-PCR survey revealed that the expression levels of a few marker genes are significantly changed as a result of CPK2 expression. Mating-based split ubiquitin system (mbSUS) and bimolecular fluorescence complementation (BiFC) were used to screen and confirm the BnaCPK2 interacting proteins. We identified and confirmed that CPK2 interacted with NADPH oxidase-like respiratory burst oxidase homolog D (RbohD), but not with RbohF. Based on its function and interacting partners, we propose that BnaCPK2 plays an important role in ROS and cell death control through interacting with RbohD.
[Mh] Termos MeSH primário: Brassica napus/genética
Morte Celular/genética
Proteínas de Plantas/genética
Proteínas Quinases/genética
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Brassica napus/enzimologia
Clonagem Molecular
DNA de Plantas
Proteínas de Plantas/metabolismo
Proteínas Quinases/metabolismo
Análise de Sequência de DNA
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Plant); 0 (Plant Proteins); 0 (Reactive Oxygen Species); EC 2.7.- (Protein Kinases); EC 2.7.1.- (calcium-dependent protein kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  3 / 39730 MEDLINE  
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[PMID]:29200852
[Au] Autor:Hu Y; Ke L; Chen H; Zhuo M; Yang X; Zhao D; Zeng S; Xiao X
[Ad] Endereço:Department of Pharmaceutics, School of Pharmaceutical Science, South-Central University for Nationalities.
[Ti] Título:Natural material-decorated mesoporous silica nanoparticle container for multifunctional membrane-controlled targeted drug delivery.
[So] Source:Int J Nanomedicine;12:8411-8426, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:To avoid the side effects caused by nonspecific targeting, premature release, weak selectivity, and poor therapeutic efficacy of current nanoparticle-based systems used for drug delivery, we fabricated natural material-decorated nanoparticles as a multifunctional, membrane-controlled targeted drug delivery system. The nanocomposite material coated with a membrane was biocompatible and integrated both specific tumor targeting and responsiveness to stimulation, which improved transmission efficacy and controlled drug release. Mesoporous silica nanoparticles (MSNs), which are known for their biocompatibility and high drug-loading capacity, were selected as a model drug container and carrier. The membrane was established by the polyelectrolyte composite method from chitosan (CS) which was sensitive to the acidic tumor microenvironment, folic acid-modified CS which recognizes the folate receptor expressed on the tumor cell surface, and a CD receptor-targeted polysaccharide hyaluronic acid. We characterized the structure of the nanocomposite as well as the drug release behavior under the control of the pH-sensitive membrane switch and evaluated the antitumor efficacy of the system in vitro. Our results provide a basis for the design and fabrication of novel membrane-controlled nanoparticles with improved tumor-targeting therapy.
[Mh] Termos MeSH primário: Materiais Biocompatíveis/química
Sistemas de Liberação de Medicamentos
Membranas Artificiais
Nanopartículas/química
Dióxido de Silício/química
[Mh] Termos MeSH secundário: Morte Celular
Quitosana/química
Liberação Controlada de Fármacos
Endocitose
Ácido Fólico/química
Células Hep G2
Seres Humanos
Nanopartículas/ultraestrutura
Tamanho da Partícula
Porosidade
Espectroscopia de Infravermelho com Transformada de Fourier
Eletricidade Estática
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Membranes, Artificial); 7631-86-9 (Silicon Dioxide); 9012-76-4 (Chitosan); 935E97BOY8 (Folic Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S148438


  4 / 39730 MEDLINE  
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[PMID]:28452703
[Au] Autor:Shin JM; Park JH; Kim HJ; Park IH; Lee HM
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Korea University College of Medicine, Seoul, South Korea.
[Ti] Título:Cigarette smoke extract increases vascular endothelial growth factor production TLR4/ROS/MAPKs/NF-kappaB pathway in nasal fibroblast.
[So] Source:Am J Rhinol Allergy;31(2):78-84, 2017 Mar 01.
[Is] ISSN:1945-8932
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Cigarette smoke is a complex mixture of various chemical compounds, including free radicals and highly toxic compounds. Cigarette smoke exposure has been shown to be associated with chronic rhinosinusitis and tissue remodeling in upper airway. Vascular endothelial growth factor (VEGF) is one of the cytokines with a crucial role in tissue remodeling of airway. The aims of this study were to determine the effects of cigarette smoke extract (CSE) on VEGF expression and to investigate the underlying molecular mechanisms of CSE in nasal fibroblasts. METHODS: Nasal fibroblasts were stimulated with CSE. Cytotoxicity was evaluated by 3-(4,5- dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. The expression level of VEGF was measured using reverse transcription-polymerase chain reaction (RT-PCR), and enzyme-linked immunosorbent assay. Messenger RNA (mRNA) expression level of TLR4 were determined by RT-PCR. Small interfering RNA (siRNA) for TLR4 was transfected to suppress TLR4 expression. Activation of reactive oxygen species (ROS) was analyzed by using dichloro-dihydro-fluorescein diacetate assay. Mitogen-activated protein kinase (MAPK) and NF-kappaB activations were determined by using western blot and/or luciferase assay. RESULTS: CSE had no significant cytotoxic effect in nasal fibroblast up to 5%. CSE significantly increased both VEGF mRNA and protein expression dose-dependently. The down-regulation of TLR4 transcription by siRNA treatment suppressed CSE-induced expressions of both TLR4 and VEGF. Pretreatment with ROS scavengers, specific inhibitors of each MAPK, and NF-kappaB inhibitor significantly decreased CSE-induced VEGF expression. CONCLUSIONS: CSE has a stimulatory effect on VEGF expression through the TLR4, ROS, MAPK, and NF-kappaB signaling pathway in nasal fibroblasts.
[Mh] Termos MeSH primário: Fibroblastos/fisiologia
Nariz/patologia
Receptor 4 Toll-Like/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Mh] Termos MeSH secundário: Adulto
Morte Celular
Células Cultivadas
Fumar Cigarros/efeitos adversos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Regulação da Expressão Gênica
Seres Humanos
Masculino
NF-kappa B/metabolismo
RNA Interferente Pequeno/genética
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais
Receptor 4 Toll-Like/genética
Fator A de Crescimento do Endotélio Vascular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (TLR4 protein, human); 0 (Toll-Like Receptor 4); 0 (Vascular Endothelial Growth Factor A); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.2500/ajra.2017.31.4415


  5 / 39730 MEDLINE  
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[PMID]:28468916
[Au] Autor:Vujanovic L; Stahl EC; Pardee AD; Geller DA; Tsung A; Watkins SC; Gibson GA; Storkus WJ; Butterfield LH
[Ad] Endereço:University of Pittsburgh Cancer Institute, University of Pittsburgh, Pennsylvania.
[Ti] Título:Tumor-Derived α-Fetoprotein Directly Drives Human Natural Killer-Cell Activation and Subsequent Cell Death.
[So] Source:Cancer Immunol Res;5(6):493-502, 2017 Jun.
[Is] ISSN:2326-6074
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatocellular carcinoma (HCC) patients with reduced natural killer (NK)-cell numbers and function have been shown to have a poor disease outcome. Mechanisms underlying NK-cell deficiency and dysfunction in HCC patients remain largely unresolved. α-Fetoprotein (AFP) is an oncofetal antigen produced by HCC. Previous studies demonstrated that tumor-derived AFP (tAFP) can indirectly impair NK-cell activity by suppressing dendritic cell function. However, a direct tAFP effect on NK cells remains unexplored. The purpose of this study was to examine the ability of cord blood-derived AFP (nAFP) and that of tAFP to directly modulate human NK-cell activity and longevity Short-term exposure to tAFP and, especially, nAFP proteins induced a unique proinflammatory, IL2-hyperresponsive phenotype in NK cells as measured by IL1ß, IL6, and TNF secretion, CD69 upregulation, and enhanced tumor cell killing. In contrast, extended coculture with tAFP, but not nAFP, negatively affected long-term NK-cell viability. NK-cell activation was directly mediated by the AFP protein itself, whereas their viability was affected by hydrophilic components within the low molecular mass cargo that copurified with tAFP. Identification of the distinct impact of circulating tAFP on NK-cell function and viability may be crucial to developing a strategy to ameliorate HCC patient NK-cell functional deficits. .
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/imunologia
Células Matadoras Naturais/imunologia
Neoplasias Hepáticas/imunologia
alfa-Fetoproteínas/imunologia
[Mh] Termos MeSH secundário: Morte Celular
Linhagem Celular Tumoral
Proliferação Celular
Células Cultivadas
Citocinas/imunologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AFP protein, human); 0 (Cytokines); 0 (alpha-Fetoproteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1158/2326-6066.CIR-16-0216


  6 / 39730 MEDLINE  
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[PMID]:28463417
[Au] Autor:Tolosa L; Gómez-Lechón MJ; Donato MT
[Ad] Endereço:Unidad de Hepatología Experimental, Instituto de Investigación Sanitaria La Fe (IIS-La Fe), Valencia, Spain.
[Ti] Título:A Multi-Parametric Fluorescent Assay for the Screening and Mechanistic Study of Drug-Induced Steatosis in Liver Cells in Culture.
[So] Source:Curr Protoc Toxicol;72:14.15.1-14.15.11, 2017 May 02.
[Is] ISSN:1934-9262
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human hepatic cells have been used for drug safety risk evaluations throughout early development phases. They provide rapid, cost-effective early feedback to identify drug candidates with potential hepatotoxicity. This unit presents a cell-based assay to evaluate the risk of liver damage associated with steatogenic drugs. Detailed protocols for cell exposure to test compounds and for the assessment of steatosis-related cell parameters (intracellular lipid content, reactive oxygen species production, mitochondrial impairment, and cell death) are provided. A few representative results that illustrate the utility of this procedure for the screening of drug-induced steatosis are shown. © 2017 by John Wiley & Sons, Inc.
[Mh] Termos MeSH primário: Fígado Gorduroso/induzido quimicamente
Fígado Gorduroso/patologia
Fígado/citologia
[Mh] Termos MeSH secundário: Morte Celular/efeitos dos fármacos
Células Cultivadas
Doença Hepática Induzida por Substâncias e Drogas
Hepatócitos/metabolismo
Seres Humanos
Metabolismo dos Lipídeos/efeitos dos fármacos
Mitocôndrias Hepáticas/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
Toxicologia/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/cptx.20


  7 / 39730 MEDLINE  
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[PMID]:28748404
[Au] Autor:Scariot FJ; Jahn L; Delamare APL; Echeverrigaray S
[Ad] Endereço:Institute of Biotechnology, University of Caxias do Sul, Caxias do Sul, Rio Grande Do Sul, Brazil.
[Ti] Título:Necrotic and apoptotic cell death induced by Captan on Saccharomyces cerevisiae.
[So] Source:World J Microbiol Biotechnol;33(8):159, 2017 Aug.
[Is] ISSN:1573-0972
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Captan is one of the most widely used broad-spectrum fungicide applied to control several early and late diseases of grapes, apples, and other fruits and vegetables, and as other phthalimide fungicides is defined as a multisite compound with thiol-reactivity. Captan can affect non-target organisms as yeasts, modifying microbial populations and fermentation processes. In this study, we asked whether Captan thiol-reactivity and other mechanisms are involved in acute Captan-induced cell death on aerobic growing Saccharomyces cerevisiae. Thus for, we analyze cellular protein and non-protein thiols, cell membrane integrity, reactive oxygen species accumulation, phosphatidylserine externalization, and apoptotic mutants behavior. The results showed that when submitted to acute Captan treatment most cells lost their membrane integrity and died by necrosis due to Captan reaction with thiols. However, part of the cells, even maintaining their membrane integrity, lost their culture ability. These cells showed an apoptotic behavior that may be the result of non-protein thiol depletion and consequent increase of reactive oxygen species (ROS). ROS accumulation triggers a metacaspase-dependent apoptotic cascade, as shown by the higher viability of the yca1-deleted mutant. Together, necrosis and apoptosis are responsible for the high mortality detected after acute Captan treatment of aerobically growing cells of S. cerevisiae.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Captana/farmacologia
Morte Celular/efeitos dos fármacos
Saccharomyces cerevisiae/efeitos dos fármacos
[Mh] Termos MeSH secundário: Membrana Celular/efeitos dos fármacos
Fermentação
Fungicidas Industriais/farmacologia
Viabilidade Microbiana/efeitos dos fármacos
Mutação
Necrose
Espécies Reativas de Oxigênio/metabolismo
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/crescimento & desenvolvimento
Proteínas de Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/metabolismo
Compostos de Sulfidrila/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fungicides, Industrial); 0 (Reactive Oxygen Species); 0 (Saccharomyces cerevisiae Proteins); 0 (Sulfhydryl Compounds); EOL5G26Q9F (Captan)
[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:170728
[St] Status:MEDLINE
[do] DOI:10.1007/s11274-017-2325-3


  8 / 39730 MEDLINE  
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[PMID]:28460485
[Au] Autor:Lv LX; Zhou ZX; Zhou Z; Zhang LJ; Yan R; Zhao Z; Yang LY; Bian XY; Jiang HY; Li YD; Sun YS; Xu QQ; Hu GL; Guan WJ; Li YQ
[Ad] Endereço:Institute of Pharmaceutical Biotechnology and College of Pharmaceutical Sciences, Zhejiang University, 310058 Hangzhou, China.
[Ti] Título:Hispidin induces autophagic and necrotic death in SGC-7901 gastric cancer cells through lysosomal membrane permeabilization by inhibiting tubulin polymerization.
[So] Source:Oncotarget;8(16):26992-27006, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hispidin and its derivatives are widely distributed in edible mushrooms. Hispidin is more cytotoxic to A549, SCL-1, Bel7402 and Capan-1 cancer cells than to MRC5 normal cells; by contrast, hispidin protects H9c2 cardiomyoblast cells from hydrogen peroxide-induced or doxorubicin-induced apoptosis. Consequently, further research on how hispidin affects normal and cancer cells may help treat cancer and reduce chemotherapy-induced side effects. This study showed that hispidin caused caspase-independent death in SGC-7901 cancer cells but not in GES-1 normal cells. Hispidin-induced increases in LC3-II occurred in SGC-7901 cells in a time independent manner. Cell death can be partially inhibited by treatment with ATG5 siRNA but not by autophagy or necroptosis inhibitors. Ultrastructural evidence indicated that hispidin-induced necrotic cell death involved autophagy. Hispidin-induced lysosomal membrane permeabilization (LMP) related to complex cell death occurred more drastically in SGC-7901 cells than in GES-1 cells. Ca2+ rather than cathepsins from LMP contributed more to cell death. Hispidin induced microtubule depolymerization, which can cause LMP, more drastically in SGC-7901 cells than in GES-1 cells. At 4.1 µM, hispidin promoted cell-free tubulin polymerization but at concentrations higher than 41 µM, hispidin inhibited polymerization. Hispidin did not bind to tubulin. Alterations in microtubule regulatory proteins, such as stathmin phosphorylation at Ser16, contributed to hispidin-induced SGC-7901 cell death. In conclusion, hispidin at concentrations higher than 41 µM may inhibit tubulin polymerization by modulating microtubule regulatory proteins, such as stathmin, causing LMP and complex SGC-7901 cell death. This mechanism suggests a promising novel treatment for human cancer.
[Mh] Termos MeSH primário: Autofagia/efeitos dos fármacos
Membranas Intracelulares/efeitos dos fármacos
Lisossomos/metabolismo
Multimerização Proteica/efeitos dos fármacos
Pironas/farmacologia
Tubulina (Proteína)/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Caspases/metabolismo
Morte Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Seres Humanos
Microtúbulos/química
Microtúbulos/metabolismo
Óxido Nítrico/biossíntese
Permeabilidade
Fosforilação
Estatmina/metabolismo
Tubulina (Proteína)/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pyrones); 0 (STMN1 protein, human); 0 (Stathmin); 0 (Tubulin); 31C4KY9ESH (Nitric Oxide); EC 3.4.22.- (Caspases); SSJ18CG55E (hispidin)
[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.15935


  9 / 39730 MEDLINE  
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[PMID]:29331752
[Au] Autor:Reddy TS; Privér SH; Mirzadeh N; Bhargava SK
[Ad] Endereço:Centre for Advanced Materials & Industrial Chemistry (CAMIC), School of Science, RMIT University, GPO BOX 2476, Melbourne 3001, Australia.
[Ti] Título:Synthesis of gold(I) phosphine complexes containing the 2-BrC F PPh ligand: Evaluation of anticancer activity in 2D and 3D spheroidal models of HeLa cancer cells.
[So] Source:Eur J Med Chem;145:291-301, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Newly synthesised mononuclear gold complexes containing the 2-BrC F PPh ligand have been fully characterised and their anticancer activity towards five human tumor [prostate (PC3), glioblastoma (U87MG), cervical (HeLa), fibrosarcoma (HT1080), ovarian (SKOV-3)] and normal human embryonic kidney (Hek-293T) cell lines investigated. Some of the synthesised gold complexes displayed higher cytotoxicity than cisplatin towards PC-3, HeLa and U87MG cells and inhibited the thioredoxin reductase (TrxR) enzyme, which is considered a potential target for new compounds in cancer treatment. The more physiologically relevant tumor spheroid assay demonstrated the superior potency of these gold phosphine complexes in inhibiting the growth of cervical carcinoma cell line HeLa (3D) spheroidal models. The mechanism of cell death was shown to be apoptotic cell death through cell cycle arrest, mitochondrial membrane depolarisation and increased ROS production.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Modelos Biológicos
Compostos Organoáuricos/farmacologia
Fosfinas/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Morte Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Cristalografia por Raios X
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Células HeLa
Seres Humanos
Ligantes
Modelos Moleculares
Estrutura Molecular
Compostos Organoáuricos/síntese química
Compostos Organoáuricos/química
Fosfinas/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-BrC6F4PPh2); 0 (Antineoplastic Agents); 0 (Ligands); 0 (Organogold Compounds); 0 (Phosphines); FW6947296I (phosphine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180115
[St] Status:MEDLINE


  10 / 39730 MEDLINE  
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[PMID]:29329002
[Au] Autor:Durdagi S; Aksoydan B; Erol I; Kantarcioglu I; Ergun Y; Bulut G; Acar M; Avsar T; Liapakis G; Karageorgos V; Salmas RE; Sergi B; Alkhatib S; Turan G; Yigit BN; Cantasir K; Kurt B; Kilic T
[Ad] Endereço:Computational Biology and Molecular Simulations Laboratory, Department of Biophysics, School of Medicine, Bahcesehir University (BAU), Istanbul, Turkey; Neuroscience Program, Graduate School of Health Sciences, Bahcesehir University, Istanbul, Turkey. Electronic address: serdar.durdagi@med.bau.edu.t
[Ti] Título:Integration of multi-scale molecular modeling approaches with experiments for the in silico guided design and discovery of novel hERG-Neutral antihypertensive oxazalone and imidazolone derivatives and analysis of their potential restrictive effects on cell proliferation.
[So] Source:Eur J Med Chem;145:273-290, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:AT1 antagonists is the most recent drug class of molecules against hypertension and they mediate their actions through blocking detrimental effects of angiotensin II (A-II) when acts on type I (AT1) A-II receptor. The effects of AT1 antagonists are not limited to cardiovascular diseases. AT1 receptor blockers may be used as potential anti-cancer agents - due to the inhibition of cell proliferation stimulated by A-II. Therefore, AT1 receptors and the A-II biosynthesis mechanisms are targets for the development of new synthetic drugs and therapeutic treatment of various cardiovascular and other diseases. In this work, multi-scale molecular modeling approaches were performed and it is found that oxazolone and imidazolone derivatives reveal similar/better interaction energy profiles compared to the FDA approved sartan molecules at the binding site of the AT1 receptor. In silico-guided designed hit molecules were then synthesized and tested for their binding affinities to human AT1 receptor in radioligand binding studies, using [ I-Sar -Ile ] AngII. Among the compounds tested, 19d and 9j molecules bound to receptor in a dose response manner and with relatively high affinities. Next, cytotoxicity and wound healing assays were performed for these hit molecules. Since hit molecule 19d led to deceleration of cell motility in all three cell lines (NIH3T3, A549, and H358) tested in this study, this molecule is investigated in further tests. In two cell lines (HUVEC and MCF-7) tested, 19d induced G2/M cell cycle arrest in a concentration dependent manner. Adherent cells detached from the plates and underwent cell death possibly due to apoptosis at 19d concentrations that induced cell cycle arrest.
[Mh] Termos MeSH primário: Anti-Hipertensivos/farmacologia
Antineoplásicos/farmacologia
Descoberta de Drogas
Canais de Potássio Éter-A-Go-Go/antagonistas & inibidores
Imidazóis/farmacologia
Oxazolona/farmacologia
[Mh] Termos MeSH secundário: Animais
Anti-Hipertensivos/síntese química
Anti-Hipertensivos/química
Antineoplásicos/síntese química
Antineoplásicos/química
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Morte Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Canais de Potássio Éter-A-Go-Go/metabolismo
Seres Humanos
Imidazóis/síntese química
Imidazóis/química
Camundongos
Modelos Moleculares
Estrutura Molecular
Células NIH 3T3
Oxazolona/síntese química
Oxazolona/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Antineoplastic Agents); 0 (Ether-A-Go-Go Potassium Channels); 0 (Imidazoles); 0 (KCNH1 protein, human); 0 (imidazolone); 15646-46-5 (Oxazolone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE



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