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  1 / 7017 MEDLINE  
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[PMID]:28458167
[Au] Autor:Fan TT; Feng XY; Yang YZ; Gao F; Liu Q
[Ad] Endereço:Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China; Department of Emergency, Chengdu First People's Hospital, Sichuan 610016, PR China.
[Ti] Título:Downregulation of PI3K-γ in a mouse model of sepsis-induced myocardial dysfunction.
[So] Source:Cytokine;96:208-216, 2017 08.
[Is] ISSN:1096-0023
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A key component during sepsis is the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, of which the PI3K-γ isoform is a major regulator in many inflammatory responses. However, the role of PI3K-γ in the development of sepsis-induced myocardial dysfunction (SIMD) is unknown. In this study, we established a model of SIMD induced by lipopolysaccharide (LPS), subsequently used the selective inhibitor LY294002 and AS605240 to block the effect of PI3K and PI3K-γ, respectively. Cardiac function was evaluated by echocardiography, hearts were obtained for histological and protein expression examinations. ELISA was used to measure the serum levels of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), cardiac troponin I (cTnI) and heart-type fatty acid binding protein (H-FABP). LPS-treated mice showed an increase to cardiac inflammation, myocardial damage and production of TNF-α, IL-6, NF-κB, cTnI and H-FABP. Administration of AS605240 to LPS-treated mice reduced some patho-physiological characteristics of SIMD and reduced TNF-α, IL-6, cTnI and H-FABP production. However, administration of LY294002 did not improve those same conditions. The results showed that PI3K-γ is likely a crucial element in SIMD by regulating the PI3K/Akt pathway, and become a new marker of myocardial injury. Inhibition of PI3K-γ might be a potential therapeutic target in SIMD.
[Mh] Termos MeSH primário: Cardiomiopatias/metabolismo
Classe II de Fosfatidilinositol 3-Quinases/metabolismo
Sepse/complicações
[Mh] Termos MeSH secundário: Animais
Cardiomiopatias/genética
Cardiomiopatias/fisiopatologia
Cromonas/administração & dosagem
Classe II de Fosfatidilinositol 3-Quinases/genética
Citocinas/sangue
Modelos Animais de Doenças
Regulação para Baixo
Interleucina-6/biossíntese
Lipopolissacarídeos/administração & dosagem
Camundongos
Morfolinas/administração & dosagem
Miocárdio/patologia
Quinoxalinas/administração & dosagem
Quinoxalinas/uso terapêutico
Transdução de Sinais/efeitos dos fármacos
Tiazolidinedionas/administração & dosagem
Tiazolidinedionas/uso terapêutico
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-quinoxalin-6-ylmethylenethiazolidine-2,4-dione); 0 (Chromones); 0 (Cytokines); 0 (Interleukin-6); 0 (Lipopolysaccharides); 0 (Morpholines); 0 (Quinoxalines); 0 (Thiazolidinediones); 0 (Tumor Necrosis Factor-alpha); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.137 (Class II Phosphatidylinositol 3-Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  2 / 7017 MEDLINE  
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[PMID]:29208524
[Au] Autor:Wang G; Chen M; Qiu J; Xie Z; Cao A
[Ad] Endereço:Provincial Key Laboratory of Pharmaceutics in Guizhou Province, Guizhou Medical University, 4 Beijing Road, Guiyang 550004, China; School of Pharmacy, Guizhou Medical University, 4 Beijing Road, Guiyang 550004, China; National Engineering Research Center of Miao's Medicines, 4 Beijing Road, Guiyang
[Ti] Título:Synthesis, in vitro α-glucosidase inhibitory activity and docking studies of novel chromone-isatin derivatives.
[So] Source:Bioorg Med Chem Lett;28(2):113-116, 2018 01 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A novel series of chromone-isatin derivatives 6a-6p were designed, synthesized and characterized by H NMR, C NMR and HRMS. These novel synthetic compounds were evaluated for inhibitory activity against yeast α-glucosidase enzyme. The results of biological test have shown that all tested compounds exhibited excellent to potent inhibitory activity in the range of IC = 3.18 ±â€¯0.12-16.59 ±â€¯0.17 µM as compared to the standard drug acarbose (IC = 817.38 ±â€¯6.27 µM). Compound 6j (IC = 3.18 ±â€¯0.12 µM) with a hydroxyl group at the 7-position of chromone and a 4-bromobenzyl group at the N1-positions of isatin, was found to be the most active compound among the series. Furthermore, molecular docking study was performed to help understand binding interactions of the most active analogs with α-glucosidase enzyme. These results indicated that this class of compounds had potential for the development of anti-diabetic agents.
[Mh] Termos MeSH primário: Cromonas/farmacologia
Inibidores de Glicosídeo Hidrolases/farmacologia
Isatina/farmacologia
Simulação de Acoplamento Molecular
alfa-Glucosidases/metabolismo
[Mh] Termos MeSH secundário: Cromonas/química
Relação Dose-Resposta a Droga
Inibidores de Glicosídeo Hidrolases/síntese química
Inibidores de Glicosídeo Hidrolases/química
Isatina/química
Estrutura Molecular
Saccharomyces cerevisiae/enzimologia
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chromones); 0 (Glycoside Hydrolase Inhibitors); 82X95S7M06 (Isatin); EC 3.2.1.20 (alpha-Glucosidases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


  3 / 7017 MEDLINE  
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[PMID]:29374700
[Au] Autor:Sakagami H; Okudaira N; Uesawa Y; Takao K; Kagaya H; Sugita Y
[Ad] Endereço:Meikai University Research Institute of Odontology (M-RIO), Meikai University School of Dentistry, Saitama, Japan sakagami@dent.meikai.ac.jp.
[Ti] Título:Quantitative Structure-Cytotoxicity Relationship of 2-Azolylchromones.
[So] Source:Anticancer Res;38(2):763-770, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Twenty-four 2-azolylchromones were subjected to quantitative structure-activity relationship (QSAR) analysis based on their cytotoxicity and tumor specificity, in order to find their new biological activities. MATERIALS AND METHODS: Cytotoxicity against two human oral squamous cell carcinoma cell lines and two human normal oral mesenchymal cells was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method. Tumor specificity (TS) was evaluated by the ratio of the mean 50% cytotoxic concentration (CC ) against oral cells to that against oral squamous cell carcinoma cell lines. Potency-selectivity expression (PSE) value was calculated by dividing the TS value by CC against tumor cells. Apoptosis markers were detected by western blot analysis. Physicochemical, structural and quantum-chemical parameters were calculated based on the conformations optimized by force-field minimization. RESULTS: Three sets of 4H-1-benzopyran-4-ones with indole ring showed much higher TS values than those with pyrrole, pyrazole, imidazole, 1,2,4-triazole, 1,2,3-triazole, indazole and benzimidazole rings. Among those with an indole ring, the compound having a 6-methoxy group, that exhibited the highest cytotoxicity, yielded one to three-order higher PSE values to compared with other groups of compounds. Western blot analysis demonstrated that this compound stimulated the cleavage of caspase-3, suggesting the induction of apoptosis. QSAR analysis demonstrated that TS values were correlated with 3D shape, polarizability, ionization potential and lipophilicity. CONCLUSION: Chemical modification of the lead compound may be a potential choice for designing a new type of anticancer drug.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Cromonas/química
Cromonas/farmacologia
Relação Quantitativa Estrutura-Atividade
[Mh] Termos MeSH secundário: Antineoplásicos/química
Carcinoma de Células Escamosas/tratamento farmacológico
Carcinoma de Células Escamosas/patologia
Seres Humanos
Neoplasias Bucais/tratamento farmacológico
Neoplasias Bucais/patologia
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Chromones)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  4 / 7017 MEDLINE  
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[PMID]:29287093
[Au] Autor:Hossain ME; Matsuzaki K; Katakura M; Sugimoto N; Mamun AA; Islam R; Hashimoto M; Shido O
[Ad] Endereço:Department of Environmental Physiology, Faculty of Medicine, Shimane University, Enya-cho, Izumo, Japan.
[Ti] Título:Direct exposure to mild heat promotes proliferation and neuronal differentiation of neural stem/progenitor cells in vitro.
[So] Source:PLoS One;12(12):e0190356, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heat acclimation in rats is associated with enhanced neurogenesis in thermoregulatory centers of the hypothalamus. To elucidate the mechanisms for heat acclimation, we investigated the effects of direct mild heat exposure on the proliferation and differentiation of neural stem/progenitor cells (NSCs/NPCs). The NSCs/NPCs isolated from forebrain cortices of 14.5-day-old rat fetuses were propagated as neurospheres at either 37.0°C (control) or 38.5°C (mild heat exposure) for four days, and the effects on proliferation were investigated by MTS cell viability assay, measurement of neurosphere diameter, and counting the total number of cells. The mRNA expressions of heat shock proteins (HSPs) and brain-derived neurotrophic factor (BDNF), cAMP response element-binding (CREB) protein and Akt phosphorylation levels, and intracellular reactive oxygen species (ROS) levels were analyzed using real time PCR, Western blotting and CM-H2DCFDA assay respectively. Heat exposure under proliferation condition increased NSC/NPC viability, neurosphere diameter, and cell count. BDNF mRNA expression, CREB phosphorylation, and ROS level were also increased by heat exposure. Heat exposure increased HSP27 mRNA expression concomitant with enhanced p-Akt level. Moreover, treatment with LY294002 (a PI3K inhibitor) abolished the effects of heat exposure on NSC/NPC proliferation. Furthermore, heat exposure under differentiation conditions increased the proportion of cells positive for Tuj1 (a neuronal marker). These findings suggest that mild heat exposure increases NSC/NPC proliferation, possibly through activation of the Akt pathway, and also enhances neuronal differentiation. Direct effects of temperature on NSCs/NPCs may be one of the mechanisms involved in hypothalamic neurogenesis in heat-acclimated rats. Such heat-induced neurogenesis could also be an effective therapeutic strategy for neurodegenerative diseases.
[Mh] Termos MeSH primário: Diferenciação Celular
Proliferação Celular
Temperatura Alta
Células-Tronco Neurais/citologia
Neurônios/citologia
[Mh] Termos MeSH secundário: Animais
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Proteína de Ligação a CREB/metabolismo
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Cromonas/farmacologia
Proteínas de Choque Térmico/metabolismo
Morfolinas/farmacologia
Células-Tronco Neurais/metabolismo
Neurônios/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Ratos
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (Chromones); 0 (Heat-Shock Proteins); 0 (Morpholines); 0 (Reactive Oxygen Species); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (Crebbp protein, rat); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190356


  5 / 7017 MEDLINE  
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[PMID]:28448439
[Au] Autor:Li TM; Liu SC; Huang YH; Huang CC; Hsu CJ; Tsai CH; Wang SW; Tang CH
[Ad] Endereço:School of Chinese Medicine, China Medical University, Taichung 40402, Taiwan. leedemaw@mail.cmu.edu.tw.
[Ti] Título:YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 27.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:YKL-40, also known as human cartilage glycoprotein-39 or chitinase-3-like-1, is a pro-inflammatory protein that is highly expressed in rheumatoid arthritis (RA) patients. Angiogenesis is a critical step in the pathogenesis of RA, promoting the infiltration of inflammatory cells into joints and providing oxygen and nutrients to RA pannus. In this study, we examined the effects of YKL-40 in the production of the pro-inflammatory cytokine interleukin-18 (IL-18), and the stimulation of angiogenesis and accumulation of osteoblasts. We observed that YKL-40 induces IL-18 production in osteoblasts and thereby stimulates angiogenesis of endothelial progenitor cells (EPCs). We found that this process occurs through the suppression of miR-590-3p via the focal adhesion kinase (FAK)/PI3K/Akt signaling pathway. YKL-40 inhibition reduced angiogenesis in in vivo models of angiogenesis: the chick embryo chorioallantoic membrane (CAM) and Matrigel plug models. We report that YKL-40 stimulates IL-18 expression in osteoblasts and facilitates EPC angiogenesis.
[Mh] Termos MeSH primário: Proteína 1 Semelhante à Quitinase-3/metabolismo
Interleucina-18/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Animais
Antagomirs/metabolismo
Artrite Reumatoide/patologia
Sequência de Bases
Movimento Celular/efeitos dos fármacos
Células Cultivadas
Proteína 1 Semelhante à Quitinase-3/antagonistas & inibidores
Proteína 1 Semelhante à Quitinase-3/genética
Cromonas/farmacologia
Células Progenitoras Endoteliais/citologia
Células Progenitoras Endoteliais/efeitos dos fármacos
Células Progenitoras Endoteliais/metabolismo
Proteína-Tirosina Quinases de Adesão Focal/metabolismo
Seres Humanos
Interleucina-18/antagonistas & inibidores
Interleucina-18/genética
Camundongos
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Morfolinas/farmacologia
Neovascularização Fisiológica/efeitos dos fármacos
Osteoblastos/citologia
Osteoblastos/efeitos dos fármacos
Osteoblastos/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/genética
Proteínas Recombinantes/farmacologia
Alinhamento de Sequência
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antagomirs); 0 (CHI3L1 protein, human); 0 (Chitinase-3-Like Protein 1); 0 (Chromones); 0 (Interleukin-18); 0 (MIRN590 microRNA, human); 0 (MicroRNAs); 0 (Morpholines); 0 (Recombinant Proteins); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


  6 / 7017 MEDLINE  
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[PMID]:29216640
[Au] Autor:Sun YZ; Cai N; Liu NN
[Ti] Título:Celecoxib Down-Regulates the Hypoxia-Induced Expression of HIF-1α and VEGF Through the PI3K/AKT Pathway in Retinal Pigment Epithelial Cells.
[So] Source:Cell Physiol Biochem;44(4):1640-1650, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The goal of this study was to detect the expression of hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF) in human retinal pigmented epithelial (RPE) cells treated with celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, under hypoxic and normoxic conditions and to explore the signaling mechanism involved in regulating the hypoxia-induced expression of HIF-1α and VEGF in RPE cells. METHODS: D407 cells were cultured in normoxic or hypoxic conditions, with or without celecoxib or a PI3K inhibitor (LY294002). The anti-proliferative effect of celecoxib was assessed using the MTT assay. RT-PCR, Western blotting and ELISA were performed to detect the levels of PI3K, phosphorylated AKT (p-AKT), HIF-1α, VEGF and COX-2. RESULTS: Celecoxib inhibited the proliferation of RPE cells in a dose-dependent manner. Celecoxib suppressed the expression of VEGF at both the mRNA and protein levels and decreased HIF-1α protein expression. HIF-1α activation was regulated by the PI3K/AKT pathway. The celecoxib-induced down-regulation of HIF-1α and VEGF required the suppression of the hypoxia-induced PI3K/AKT pathway. However, the down-regulation of COX-2 did not occur in cells treated with celecoxib. CONCLUSIONS: The antiangiogenic effects of celecoxib in RPE cells under hypoxic conditions resulted from the inhibition of HIF-1α and VEGF expression, which may be partly mediated by a COX-2-independent, PI3K/AKT-dependent pathway.
[Mh] Termos MeSH primário: Celecoxib/farmacologia
Hipóxia Celular
Inibidores de Ciclo-Oxigenase 2/farmacologia
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Proliferação Celular/efeitos dos fármacos
Cromonas/farmacologia
Ciclo-Oxigenase 2/química
Ciclo-Oxigenase 2/metabolismo
Regulação para Baixo/efeitos dos fármacos
Células Epiteliais/citologia
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Morfolinas/farmacologia
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
RNA Mensageiro/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromones); 0 (Cyclooxygenase 2 Inhibitors); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Morpholines); 0 (RNA, Messenger); 0 (Vascular Endothelial Growth Factor A); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 1.14.99.1 (Cyclooxygenase 2); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); JCX84Q7J1L (Celecoxib)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1159/000485764


  7 / 7017 MEDLINE  
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[PMID]:29176314
[Au] Autor:Wang H; Deng X; Zhang J; Ou Z; Mai J; Ding S; Huo S
[Ad] Endereço:Department of Radiation Oncology, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
[Ti] Título:Elevated Expression of Zinc Finger Protein 703 Promotes Cell Proliferation and Metastasis through PI3K/AKT/GSK-3ß Signalling in Oral Squamous Cell Carcinoma.
[So] Source:Cell Physiol Biochem;44(3):920-934, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Zinc finger protein 703 (ZNF703), initially identified as a novel oncogene in human breast cancer, is a member of the NET/NlZ family of zinc finger transcription factors. It is recognized that the overexpression of ZNF703 is associated with various types of human cancers, but the role and molecular mechanism of ZNF703 in oral squamous cell carcinoma (OSCC) are unknown. METHODS: ZNF703 expression levels were examined in OSCC tissues and non-cancerous tissues by qRT-PCR and immunohistochemistry (IHC). The molecular mechanisms of ZNF703 and its effects on cell growth and metastasis were explored in vitro and in vivo using the CCK8 assay, colony formation assay, cell cycle analysis, migration and invasion assays, wound-healing assay, western blotting and xenograft experiments in nude mice. RESULTS: In this study, ZNF703 was found to be upregulated in OSCC tissues compared to that in normal tissues at both mRNA and protein levels, and its expression level was closely correlated with the overall survival of patients with OSCC. Silencing of the ZNF703 gene in OSCC cells significantly inhibited cell growth and metastasis in vitro and in vivo. Conversely, the overexpression of ZNF703 in OSCC cells promoted cancer growth and metastasis in vitro. Mechanistically, ZNF703 activated the PI3K/AKT/GSK-3ß signalling pathway and its downstream effectors, thus regulating the cell cycle and epithelial-mesenchymal transition (EMT). Furthermore, the promotive effects of ZNF703 on cellular proliferation and metastasis could be rescued by LY294002 (a PI3K-specific inhibitor) and MK2206 (an Akt-specific inhibitor). CONCLUSION: The results show that ZNF703 promotes cell growth and metastasis through PI3K/Akt/GSK-3ß signalling in OSCC and that it may be a promising target in the treatment of patients with OSCC.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/patologia
Proteínas de Transporte/metabolismo
Glicogênio Sintase Quinase 3 beta/metabolismo
Neoplasias Bucais/patologia
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
[Mh] Termos MeSH secundário: Animais
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/mortalidade
Proteínas de Transporte/antagonistas & inibidores
Proteínas de Transporte/genética
Pontos de Checagem do Ciclo Celular
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Cromonas/farmacologia
Transição Epitelial-Mesenquimal
Feminino
Compostos Heterocíclicos com 3 Anéis/farmacologia
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Masculino
Camundongos
Camundongos Nus
Microscopia de Fluorescência
Meia-Idade
Morfolinas/farmacologia
Neoplasias Bucais/metabolismo
Neoplasias Bucais/mortalidade
Imagem Óptica
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Transdução de Sinais
Transplante Heterólogo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Chromones); 0 (Heterocyclic Compounds, 3-Ring); 0 (MK 2206); 0 (Morpholines); 0 (RNA, Small Interfering); 0 (ZNF703 protein, human); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485360


  8 / 7017 MEDLINE  
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[PMID]:29202319
[Au] Autor:Yang Y; Chen HQ; Kong FD; Zhou LM; Li W; Dong WH; Chen ZB; Mei WL; Dai HF
[Ad] Endereço:Key Laboratory of Biology and Genetic Resources of Tropical Crops, Ministry of Agriculture, Institute of Tropical Bioscience and Biotechnology, Chinese Academy of Tropical Agricultural Sciences, Haikou, 571101, PR China; College of Life Science and Technology, Heilongjiang Bayi Agricultural Universi
[Ti] Título:Dimeric sesquiterpenoid-4H-chromone derivatives from agarwood of Aquilaria crassna and their cytotoxicity.
[So] Source:Phytochemistry;145:207-213, 2018 Jan.
[Is] ISSN:1873-3700
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Six previously undescribed uncommon ester-bonded dimeric compounds (aquilacrassnins A-F) containing a sesquiterpenoid and a 5,6,7,8-tetrahydroxy-2-(2-phenylethyl)-5,6,7,8-tetrahydro -4H-chromone units were isolated from the EtOAc extract of agarwood originating from Aquilaria crassna. Their structures were elucidated by spectroscopic (NMR, UV, IR, MS, and ECD) methods. All the compounds were tested for AChE inhibitory activity and cytotoxicity against K562, BEL-7402, SGC-7901, Hela, and A549 tumor cell lines. The results showed that aquilacrassnin A, B, and E exhibited weak cytotoxicity against the five tested cell lines, whereas all the compounds were inactive against AChE.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Cromonas/farmacologia
Thymelaeaceae/química
[Mh] Termos MeSH secundário: Antineoplásicos Fitogênicos/química
Antineoplásicos Fitogênicos/isolamento & purificação
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Cromonas/química
Cromonas/isolamento & purificação
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Estrutura Molecular
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Chromones); 0 (aquilacrassnin A); 0 (aquilacrassnin B); 0 (aquilacrassnin E)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  9 / 7017 MEDLINE  
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[PMID]:28460819
[Au] Autor:Luo G; Chen M; Lyu W; Zhao R; Xu Q; You Q; Xiang H
[Ad] Endereço:Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing 210009, PR China.
[Ti] Título:Design, synthesis, biological evaluation and molecular docking studies of novel 3-aryl-4-anilino-2H-chromen-2-one derivatives targeting ERα as anti-breast cancer agents.
[So] Source:Bioorg Med Chem Lett;27(12):2668-2673, 2017 06 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The estrogen receptor (ER) has played an important role in breast cancer development and progression and is a central target for anticancer drug discovery. In order to develop novel selective ERα modulators (SERMs), we designed and synthesized 18 novel 3-aryl-4-anilino-2H-chromen-2-one derivatives based on previously reported lead compounds. The biological results indicated that most of the compounds presented potent ERα binding affinity and possessed better anti-proliferative activities against MCF-7 and Ishikawa cell lines than the positive control tamoxifen. The piperidyl substituted compounds such as 16d and 18d demonstrated strong ERα binding affinities and excellent anti-proliferative activities respectively. Compound 18d displayed the most potent ERα binding affinity with RBA value of 2.83%, while 16d exhibited the best anti-proliferative activity against MCF-7 cells with IC value of 4.52±2.47µM. Further molecular docking studies were also carried out to investigate binding pattern of the newly synthesized compounds with ERα. All these results together with the structure-activity relationships (SARs) indicated that these 3-aryl-4-anilino-2H-chromen-2-one derivatives with basic side chain could serve as promising leads for further optimization as novel SERMs.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Cromonas/farmacologia
Desenho de Drogas
Receptor alfa de Estrogênio/antagonistas & inibidores
Simulação de Acoplamento Molecular
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Cromonas/síntese química
Cromonas/química
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Receptor alfa de Estrogênio/metabolismo
Seres Humanos
Células MCF-7
Estrutura Molecular
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Chromones); 0 (Estrogen Receptor alpha)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  10 / 7017 MEDLINE  
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[PMID]:28457756
[Au] Autor:Kobayashi Y; Saito Y; Goto M; Nakagawa-Goto K
[Ad] Endereço:School of Pharmaceutical Sciences, College of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa 920-1192, Japan.
[Ti] Título:Antitubulin effects of aminobenzothiophene-substituted triethylated chromones.
[So] Source:Bioorg Med Chem Lett;27(12):2731-2735, 2017 06 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In the course of our continuing studies on the 2-(benzo[b]thiophene-3'-yl)-6,8,8-triethyldesmosdumotin B (TEDB-TB) series, we designed and synthesized nine amino-TEDB-TB derivatives to improve pharmaceutical properties, identify structure activity relationships, and discover novel antitubulin agents. Among all newly synthesized amino-TEDB-TBs, the 5'- and 6'-amino derivatives, 6 and 7, exhibited significant antiproliferative activity against five human tumor cell lines, including an MDR subline overexpressing P-gp. The IC values of 0.50-1.01µM were 3-6 times better than those of previously reported hydroxy-TEDB-TBs. Compounds 6 and 7 inhibited tubulin polymerization, induced both depolymerization of interphase microtubules and multiple spindle formations, and caused cell arrest at prometaphase. Among all compounds, compound 7 scored best pharmaceutically with LogP 2.11 and biologically with greater antiproliferative activity and induction of cell cycle arrest at prometaphase.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Cromonas/farmacologia
Flavonoides/farmacologia
Tiofenos/farmacologia
Tubulina (Proteína)/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Cromonas/síntese química
Cromonas/química
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Flavonoides/síntese química
Flavonoides/química
Seres Humanos
Estrutura Molecular
Polimerização/efeitos dos fármacos
Prometáfase/efeitos dos fármacos
Relação Estrutura-Atividade
Tiofenos/síntese química
Tiofenos/química
Moduladores de Tubulina
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (2-(6'-aminobenzo(b)thiophen-3'-yl)-6,8,8-triethyldesmosdumotin B); 0 (Antineoplastic Agents); 0 (Chromones); 0 (Flavonoids); 0 (Thiophenes); 0 (Tubulin); 0 (Tubulin Modulators)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE



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