Base de dados : MEDLINE
Pesquisa : D12.776.826.701.250 [Categoria DeCS]
Referências encontradas : 1356 [refinar]
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[PMID]:28642153
[Au] Autor:Miro Estruch I; Melchers D; Houtman R; de Haan LHJ; Groten JP; Louisse J; Rietjens IMCM
[Ad] Endereço:Division of Toxicology, Wageningen University, Stippeneng 4, 6708 WE Wageningen, The Netherlands. Electronic address: ignacio.miroestruch@wur.nl.
[Ti] Título:Characterization of the differential coregulator binding signatures of the Retinoic Acid Receptor subtypes upon (ant)agonist action.
[So] Source:Biochim Biophys Acta;1865(9):1195-1206, 2017 09.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Retinoic Acid Receptor alpha (RARα/NR1B1), Retinoic Acid Receptor beta (RARß/NR1B2) and Retinoic Acid Receptor gamma (RARγ/NR1B3) are transcription factors regulating gene expression in response to retinoids. Within the RAR genomic pathways, binding of RARs to coregulators is a key intermediate regulatory phase. However, ligand-dependent interactions between the wide variety of coregulators that may be present in a cell and the different RAR subtypes are largely unknown. The aim of this study is to characterize the coregulator binding profiles of RARs in the presence of the pan-agonist all-trans-Retinoic Acid (AtRA); the subtype-selective agonists Am80 (RARα), CD2314 (RARß) and BMS961 (RARγ); and the antagonist Ro415253. To this end, we used a microarray assay for coregulator-nuclear receptor interactions to assess RAR binding to 154 motifs belonging to >60 coregulators. The results revealed a high number of ligand-dependent RAR-coregulator interactions among all RAR variants, including many binding events not yet described in literature. Next, this work confirmed a greater ligand-independent activity of RARß compared to the other RAR subtypes based on both higher basal and lower ligand-driven coregulator binding. Further, several coregulator motifs showed selective binding to a specific RAR subtype. Next, this work showed that subtype-selective agonists can be successfully discriminated by using coregulator binding assays. Finally this study demonstrated the possible applications of a coregulator binding assay as a tool to discriminate between agonistic/antagonistic actions of ligands. The RAR-coregulator interactions found will be of use to direct further studies to better understand the mechanisms driving the eventual actions of retinoids.
[Mh] Termos MeSH primário: Receptores do Ácido Retinoico/química
Receptor alfa de Ácido Retinoico/química
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Antracenos/farmacologia
Benzoatos/farmacologia
Sítios de Ligação
Análise Serial de Proteínas
Ligação Proteica
Domínios Proteicos
Receptores do Ácido Retinoico/agonistas
Receptores do Ácido Retinoico/antagonistas & inibidores
Proteínas Recombinantes/metabolismo
Elementos de Resposta
Receptor alfa de Ácido Retinoico/agonistas
Receptor alfa de Ácido Retinoico/antagonistas & inibidores
Retinoides/farmacologia
Relação Estrutura-Atividade
Tetra-Hidronaftalenos/farmacologia
Tiofenos/farmacologia
Tretinoína/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anthracenes); 0 (BMS 961); 0 (Benzoates); 0 (CD2314); 0 (Receptors, Retinoic Acid); 0 (Recombinant Proteins); 0 (Retinoic Acid Receptor alpha); 0 (Retinoids); 0 (Ro 415253); 0 (Tetrahydronaphthalenes); 0 (Thiophenes); 0 (retinoic acid receptor beta); 0 (retinoic acid receptor gamma); 08V52GZ3H9 (tamibarotene); 5688UTC01R (Tretinoin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE


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[PMID]:28432217
[Au] Autor:Janesick A; Tang W; Nguyen TTL; Blumberg B
[Ad] Endereço:Department of Developmental and Cell Biology, 2011 Biological Sciences 3, University of California, Irvine, CA 92697-2300, USA.
[Ti] Título:RARß2 is required for vertebrate somitogenesis.
[So] Source:Development;144(11):1997-2008, 2017 06 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During vertebrate somitogenesis, retinoic acid is known to establish the position of the determination wavefront, controlling where new somites are permitted to form along the anteroposterior body axis. Less is understood about how RAR regulates somite patterning, rostral-caudal boundary setting, specialization of myotome subdivisions or the specific RAR subtype that is required for somite patterning. Characterizing the function of RARß has been challenging due to the absence of embryonic phenotypes in murine loss-of-function studies. Using the system, we show that RARß2 plays a specific role in somite number and size, restriction of the presomitic mesoderm anterior border, somite chevron morphology and hypaxial myoblast migration. is the RAR subtype whose expression is most upregulated in response to ligand and its localization in the trunk somites positions it at the right time and place to respond to embryonic retinoid levels during somitogenesis. RARß2 positively regulates a marker of hypaxial muscle, and negatively regulates via to restrict the anterior boundaries of the presomitic mesoderm and caudal progenitor pool. These results demonstrate for the first time an early and essential role for RARß2 in vertebrate somitogenesis.
[Mh] Termos MeSH primário: Desenvolvimento Embrionário
Receptores do Ácido Retinoico/metabolismo
Somitos/embriologia
Xenopus laevis/embriologia
Xenopus laevis/metabolismo
[Mh] Termos MeSH secundário: Animais
Benzoatos/farmacologia
Biomarcadores/metabolismo
Embrião não Mamífero/efeitos dos fármacos
Embrião não Mamífero/metabolismo
Desenvolvimento Embrionário/genética
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Larva/efeitos dos fármacos
Larva/metabolismo
Mesoderma/efeitos dos fármacos
Mesoderma/embriologia
Mesoderma/metabolismo
Modelos Biológicos
Morfolinos/farmacologia
Músculos/efeitos dos fármacos
Músculos/embriologia
Músculos/metabolismo
Regiões Promotoras Genéticas/genética
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Receptores do Ácido Retinoico/genética
Receptor alfa de Ácido Retinoico/genética
Receptor alfa de Ácido Retinoico/metabolismo
Retinoides/farmacologia
Somitos/efeitos dos fármacos
Somitos/metabolismo
Tretinoína/farmacologia
Proteínas de Xenopus/genética
Proteínas de Xenopus/metabolismo
Xenopus laevis/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Benzoates); 0 (Biomarkers); 0 (Morpholinos); 0 (Protein Isoforms); 0 (Receptors, Retinoic Acid); 0 (Retinoic Acid Receptor alpha); 0 (Retinoids); 0 (Xenopus Proteins); 0 (retinoic acid receptor beta); 0 (retinoic acid receptor gamma); 5688UTC01R (Tretinoin); 71441-28-6 (4-(2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-1-propenyl)benzoic acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE
[do] DOI:10.1242/dev.144345


  3 / 1356 MEDLINE  
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[PMID]:28420180
[Au] Autor:Zhang L; Wang J; Liu L; Zheng C; Wang Y
[Ad] Endereço:School of Pharmacy, Zunyi Medical University, 201 Dalian Road, Zunyi 563003, Guizhou, China. lzhang@zmc.edu.cn.
[Ti] Título:Synthesis and Antiproliferative Activity of Novel All-Trans-Retinoic Acid-Podophyllotoxin Conjugate towards Human Gastric Cancer Cells.
[So] Source:Molecules;22(4), 2017 Apr 17.
[Is] ISSN:1420-3049
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:With the purpose of creating a multifunctional drug for gastric cancer treatment, a novel -retinoic acid ( ) conjugate with podophyllotoxin ( ) was designed and synthesized, and its in vitro antiproliferative activity was evaluated against human gastric cancer cell lines using CCK-8 assay. The conjugate, , exhibited significant anticancer activity against MKN-45 and BGC-823 cells with IC values of 0.419 ± 0.032 and 0.202 ± 0.055 µM, respectively. Moreover, efficiently triggered cell cycle arrest and induced apoptosis in MKN-45 and BGC-823 cells due to modulation of cell cycle arrest- (CDK1, CDK2, CyclinA and CyclinB1) and apoptosis- (cleaved caspase-3, -8 and -9) related proteins, respectively. Further mechanism studies revealed that could increase the expression levels of RARα and RARß, and decrease the level of RARγ in MKN-45 and BGC-823 cells. Finally, inhibited the ERK1/2 and AKT signaling in the above two cancer cell lines. More importantly, the underlying mechanisms of were similar to those of precursor but different with the other precursor . Together, the conjugate was a promising candidate for the potential treatment of human gastric cancer.
[Mh] Termos MeSH primário: Antineoplásicos/síntese química
Antineoplásicos/farmacologia
Podofilotoxina
Tretinoína
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Proteínas Reguladoras de Apoptose/genética
Proteínas Reguladoras de Apoptose/metabolismo
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Expressão Gênica
Seres Humanos
Estrutura Molecular
Podofilotoxina/química
Podofilotoxina/farmacologia
Receptor alfa de Ácido Retinoico/genética
Receptor alfa de Ácido Retinoico/metabolismo
Transdução de Sinais/efeitos dos fármacos
Neoplasias Gástricas/tratamento farmacológico
Neoplasias Gástricas/genética
Neoplasias Gástricas/metabolismo
Tretinoína/química
Tretinoína/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Apoptosis Regulatory Proteins); 0 (Cell Cycle Proteins); 0 (Retinoic Acid Receptor alpha); 5688UTC01R (Tretinoin); L36H50F353 (Podophyllotoxin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE


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[PMID]:28370816
[Au] Autor:Condron KN; Waddell JN; Claeys MC; Lemenager RP; Schoonmaker JP
[Ad] Endereço:Department of Animal Sciences, Purdue University, West Lafayette, IN, USA.
[Ti] Título:Effect of supplemental ß-carotene compared to retinyl palmitate on fatty acid profile and expression of mRNA from genes involved in vitamin A metabolism in beef feedlot cattle.
[So] Source:Anim Sci J;88(9):1380-1387, 2017 Sep.
[Is] ISSN:1740-0929
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:To examine the effects of dietary ß-carotene (ßC) or retinyl palmitate (RP) on fatty acid (FA) profile and mRNA expression, samples were collected from 24 Angus-cross calves that were allotted to four treatments consisting of RP supplemented at 2200 IU/kg, and synthetic ß-carotene (SßC) supplemented at one, five or 10 times RP. Longissimus muscle (LM) cis-9, trans-11 conjugated linoleic acid was greater in RP compared to SßC1X (P = 0.04). The polyunsaturated:saturated FA increased linearly (P = 0.04) in the LM as dietary SßC increased. Expression of ßC oxygenase 2 (ßCO2), an enzyme that cleaves ß-carotene, was greater in the LM for SßC1X compared to RP and decreased linearly as SßC increased (P ≤ 0.02). Peroxisome proliferator activated receptor γ (PPARγ) expression in the LM increased in SßC1X compared to RP (P = 0.03); however, PPARγ and retinoic acid X receptor α (RXRα) expression decreased linearly (P = 0.02) in the LM with increasing SßC. Retinoic acid receptor α (RARα) expression tended (P = 0.10) to decrease linearly in the LM with increased SßC. In conclusion, SßC supplementation increased mRNA expression of some lipogenic genes in the LM, but increasing dietary SßC inhibited their expression and tended to increase polyunsaturated FA.
[Mh] Termos MeSH primário: Bovinos/genética
Bovinos/metabolismo
Dieta/veterinária
Suplementos Nutricionais
Ácidos Graxos Insaturados/metabolismo
Expressão Gênica
Lipogênese/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Vitamina A/análogos & derivados
Vitamina A/metabolismo
beta Caroteno/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Dioxigenases/genética
Dioxigenases/metabolismo
Feminino
Ácido Linoleico/metabolismo
Masculino
Músculo Esquelético/metabolismo
PPAR gama/genética
PPAR gama/metabolismo
Receptor alfa de Ácido Retinoico/genética
Receptor alfa de Ácido Retinoico/metabolismo
Vitamina A/administração & dosagem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Unsaturated); 0 (PPAR gamma); 0 (RNA, Messenger); 0 (Retinoic Acid Receptor alpha); 01YAE03M7J (beta Carotene); 11103-57-4 (Vitamin A); 1D1K0N0VVC (retinol palmitate); 9KJL21T0QJ (Linoleic Acid); EC 1.13.11.- (Dioxygenases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1111/asj.12794


  5 / 1356 MEDLINE  
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[PMID]:28282876
[Au] Autor:Kobori M; Takahashi Y; Sakurai M; Ni Y; Chen G; Nagashimada M; Kaneko S; Ota T
[Ad] Endereço:Food Research Institute, National Agriculture and Food Resrach Organization, Tsukuba, Ibaraki 305-8642, Japan. kobori@affrc.go.jp.
[Ti] Título:Hepatic Transcriptome Profiles of Mice with Diet-Induced Nonalcoholic Steatohepatitis Treated with Astaxanthin and Vitamin E.
[So] Source:Int J Mol Sci;18(3), 2017 Mar 08.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Astaxanthin alleviates hepatic lipid accumulation and peroxidation, inflammation, and fibrosis in mice with high-cholesterol, high-cholate, and high-fat (CL) diet-induced nonalcoholic steatohepatitis (NASH) [...].
[Mh] Termos MeSH primário: Fígado/efeitos dos fármacos
Fígado/metabolismo
Hepatopatia Gordurosa não Alcoólica/etiologia
Hepatopatia Gordurosa não Alcoólica/metabolismo
Transcriptoma
Vitamina E/farmacologia
[Mh] Termos MeSH secundário: Animais
Dieta Hiperlipídica/efeitos adversos
Modelos Animais de Doenças
Fator de Iniciação 2 em Eucariotos/metabolismo
Perfilação da Expressão Gênica
Masculino
Camundongos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/genética
Mitocôndrias/metabolismo
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Hepatopatia Gordurosa não Alcoólica/patologia
PPAR alfa/metabolismo
PPAR delta/metabolismo
Mapeamento de Interação de Proteínas
Mapas de Interação de Proteínas
Receptor alfa de Ácido Retinoico/metabolismo
Transdução de Sinais/efeitos dos fármacos
Xantofilas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Eukaryotic Initiation Factor-2); 0 (PPAR alpha); 0 (PPAR delta); 0 (Retinoic Acid Receptor alpha); 0 (Xanthophylls); 1406-18-4 (Vitamin E); 8XPW32PR7I (astaxanthine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170312
[St] Status:MEDLINE


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[PMID]:28216044
[Au] Autor:Solingapuram Sai KK; Das BC; Sattiraju A; Almaguel FG; Craft S; Mintz A
[Ad] Endereço:Department of Radiology, Wake Forest School of Medicine, Winston Salem, NC, USA. Electronic address: ksolinga@wakehealth.edu.
[Ti] Título:Radiolabeling and initial biological evaluation of [ F]KBM-1 for imaging RAR-α receptors in neuroblastoma.
[So] Source:Bioorg Med Chem Lett;27(6):1425-1427, 2017 03 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Retinoic acid receptor alpha (RAR-α) plays a significant role in a number of diseases, including neuroblastoma. Children diagnosed with high-risk neuroblastoma are treated13-cis-retinoic acid, which reduces risk of cancer recurrence. Neuroblastoma cell death is mediated via RAR-α, and expression of RAR-α is upregulated after treatment. A molecular imaging probe that binds RAR-α will help clinicians to diagnose and stratify risk for patients with neuroblastoma, who could benefit from retinoid-based therapy. In this study, we report the radiolabeling, and initial in vivo evaluation of [ F]KBM-1, a novel RAR-α agonist. The radiochemical synthesis of [ F]KBM-1 was carried out through KHF assisted substitution of [ F] from aryl-substituted pinacolatoesters-based retinoid precursor. In vitro cell uptake assay in human neuroblastoma cell line showed that the uptake of [ F]KBM-1 was significantly inhibited by all three blocking agents (KBM-1, ATRA, BD4) at all the selected incubation times. Standard biodistribution in mice bearing neuroblastoma tumors demonstrated increased tumor uptake from 5min to 60min post radiotracer injection and the uptake ratios for target to non-target (tumor: muscle) increased 2.2-fold to 3.7-fold from 30min to 60min post injection. Tumor uptake in subset of 30min blocking group was 1.7-fold lower than unblocked. These results demonstrate the potential utility of [ F]KBM-1 as a RAR-α imaging agent.
[Mh] Termos MeSH primário: Benzopiranos/farmacologia
Compostos de Boro/farmacologia
Radioisótopos de Flúor/metabolismo
Neuroblastoma/metabolismo
Receptor alfa de Ácido Retinoico/metabolismo
[Mh] Termos MeSH secundário: Animais
Benzopiranos/química
Benzopiranos/farmacocinética
Compostos de Boro/química
Compostos de Boro/farmacocinética
Linhagem Celular Tumoral
Ensaios de Seleção de Medicamentos Antitumorais
Xenoenxertos
Seres Humanos
Rim/metabolismo
Fígado/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Receptor alfa de Ácido Retinoico/agonistas
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Benzopyrans); 0 (Boron Compounds); 0 (Fluorine Radioisotopes); 0 (Retinoic Acid Receptor alpha)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170221
[St] Status:MEDLINE


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[PMID]:28122350
[Au] Autor:Chen S; Sun YY; Zhang ZX; Li YH; Xu ZM; Fu WN
[Ad] Endereço:Department of Medical Genetics, China Medical University, Shenyang, 110122, P.R. China.
[Ti] Título:Transcriptional suppression of microRNA-27a contributes to laryngeal cancer differentiation via GSK-3ß-involved Wnt/ß-catenin pathway.
[So] Source:Oncotarget;8(9):14708-14718, 2017 Feb 28.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:miR-27a regulates cell differentiation in a variety of diseases. However, whether and how miR-27a participates in laryngeal cancer cell differentiation remains unknown. Therefore, we explored role and molecular mechanism of miR-27a in laryngeal cancer differentiation in the study. We found that miR-27a expression was inversely correlated with laryngeal cancer differentiation degree based on the clinical pathological diagnosis of each patient. miR-27 asignificantly rescued differentiation and inhibited ß-catenin, LEF1, OCT4 and SOX2 in Wnt/ß-catenin pathway in all-trans-retinoic acid (ATRA)-induced laryngeal cancer cells. Bindings of RARα to miR-27a and miR-27a to GSK-3ß were confirmed by ChIP and Luciferase reporter assays, respectively. In conclusion, miR-27a is a negative regulator in laryngeal cancer differentiation. RARα-mediated miR-27a transcriptional inactivation releases the inhibition of miR-27a on GSK-3ß leading to laryngeal cancer differentiation through GSK-3ß-involved Wnt/ß-catenin pathway, suggesting that miR-27a is a usefully therapeutic target at least in ATRA-induced laryngeal cancer differentiation.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Regulação Neoplásica da Expressão Gênica
Glicogênio Sintase Quinase 3 beta/genética
Neoplasias Laríngeas/genética
MicroRNAs/genética
Via de Sinalização Wnt/genética
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Western Blotting
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Feminino
Glicogênio Sintase Quinase 3 beta/metabolismo
Células HEK293
Seres Humanos
Neoplasias Laríngeas/metabolismo
Neoplasias Laríngeas/patologia
Fator 1 de Ligação ao Facilitador Linfoide/genética
Fator 1 de Ligação ao Facilitador Linfoide/metabolismo
Masculino
Meia-Idade
Fator 3 de Transcrição de Octâmero/genética
Fator 3 de Transcrição de Octâmero/metabolismo
Receptor alfa de Ácido Retinoico/genética
Receptor alfa de Ácido Retinoico/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Transcrição SOXB1/genética
Fatores de Transcrição SOXB1/metabolismo
Tretinoína/farmacologia
beta Catenina/genética
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (LEF1 protein, human); 0 (Lymphoid Enhancer-Binding Factor 1); 0 (MIRN27 microRNA, human); 0 (MicroRNAs); 0 (Octamer Transcription Factor-3); 0 (POU5F1 protein, human); 0 (RARA protein, human); 0 (Retinoic Acid Receptor alpha); 0 (SOX2 protein, human); 0 (SOXB1 Transcription Factors); 0 (beta Catenin); 5688UTC01R (Tretinoin); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.14769


  8 / 1356 MEDLINE  
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[PMID]:28049897
[Au] Autor:Kobayashi T
[Ad] Endereço:Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University.
[Ti] Título:Expression and Regulation of Tal2 during Neuronal Differentiation in P19 Cells.
[So] Source:Yakugaku Zasshi;137(1):61-71, 2017.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:T-cell acute lymphocytic leukemia 2 (Tal2) is a gene encoding a member of the basic helix-loop-helix transcription factor family, which is essential for the normal development of the mouse brain. We found that Tal2 was induced during neural differentiation in P19 cells, which are pluripotent mouse embryonal carcinoma cells that differentiate into the neural lineage upon both exposure to all-trans retinoic acid (atRA) and the formation of cell aggregation. Tal2 expression during neural differentiation in P19 cells was detected within 3 h after induction with atRA and retinoic acid receptor α (RARα). The atRA-RARα complex is known to bind to a characteristic retinoic acid response element (RARE) located in the promoter of target genes. We found a RARE-like element in the intron of Tal2. We also found a TATA-box-like element in the 5' region. The TATA-box-like element functioned as a core promoter, and TATA- box binding protein bound to this element upstream of Tal2 in P19 cells. The RARE-like element responded to atRA signaling that activated the transcription, and RARα was bound to this element in the intron of Tal2 in P19 cells. Furthermore, the interaction between these elements on Tal2 was confirmed in a chromatin immunoprecipitation assay. Because the neural differentiation of P19 cells mimics in part the development of the nervous system, P19 cells are useful for studying the mechanism underlying the role of Tal2 in neural differentiation. Further work is underway to clarify the function of Tal2 in neural differentiation using the differentiation system of P19 cells.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Fatores de Transcrição Hélice-Alça-Hélice Básicos/fisiologia
Diferenciação Celular/genética
Regulação da Expressão Gênica no Desenvolvimento/genética
Expressão Gênica/genética
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/fisiologia
Neurônios/citologia
[Mh] Termos MeSH secundário: Animais
Camundongos
Regiões Promotoras Genéticas
Receptor alfa de Ácido Retinoico
TATA Box
Tretinoína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Neoplasm Proteins); 0 (Retinoic Acid Receptor alpha); 0 (Tal2 protein, mouse); 5688UTC01R (Tretinoin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170105
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.16-00176


  9 / 1356 MEDLINE  
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[PMID]:28017614
[Au] Autor:Li Z; Weng H; Su R; Weng X; Zuo Z; Li C; Huang H; Nachtergaele S; Dong L; Hu C; Qin X; Tang L; Wang Y; Hong GM; Huang H; Wang X; Chen P; Gurbuxani S; Arnovitz S; Li Y; Li S; Strong J; Neilly MB; Larson RA; Jiang X; Zhang P; Jin J; He C; Chen J
[Ad] Endereço:Section of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, IL 60637, USA; Department of Human Genetics, University of Chicago, Chicago, IL 60637, USA.
[Ti] Título:FTO Plays an Oncogenic Role in Acute Myeloid Leukemia as a N -Methyladenosine RNA Demethylase.
[So] Source:Cancer Cell;31(1):127-141, 2017 Jan 09.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:N -Methyladenosine (m A) represents the most prevalent internal modification in mammalian mRNAs. Despite its functional importance in various fundamental bioprocesses, the studies of m A in cancer have been limited. Here we show that FTO, as an m A demethylase, plays a critical oncogenic role in acute myeloid leukemia (AML). FTO is highly expressed in AMLs with t(11q23)/MLL rearrangements, t(15;17)/PML-RARA, FLT3-ITD, and/or NPM1 mutations. FTO enhances leukemic oncogene-mediated cell transformation and leukemogenesis, and inhibits all-trans-retinoic acid (ATRA)-induced AML cell differentiation, through regulating expression of targets such as ASB2 and RARA by reducing m A levels in these mRNA transcripts. Collectively, our study demonstrates the functional importance of the m A methylation and the corresponding proteins in cancer, and provides profound insights into leukemogenesis and drug response.
[Mh] Termos MeSH primário: Adenosina/análogos & derivados
Dioxigenase FTO Dependente de alfa-Cetoglutarato/fisiologia
Leucemia Mieloide Aguda/etiologia
[Mh] Termos MeSH secundário: Adenosina/metabolismo
Apoptose
Proliferação Celular
Seres Humanos
Leucemia Mieloide Aguda/tratamento farmacológico
Leucemia Mieloide Aguda/enzimologia
Leucemia Mieloide Aguda/patologia
Metilação
Receptor alfa de Ácido Retinoico/fisiologia
Proteínas Supressoras da Sinalização de Citocinas/fisiologia
Transcriptoma
Tretinoína/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ASB2 protein, human); 0 (RARA protein, human); 0 (Retinoic Acid Receptor alpha); 0 (Suppressor of Cytokine Signaling Proteins); 1867-73-8 (N(6)-methyladenosine); 5688UTC01R (Tretinoin); EC 1.14.11.33 (Alpha-Ketoglutarate-Dependent Dioxygenase FTO); EC 1.14.11.33 (FTO protein, human); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161227
[St] Status:MEDLINE


  10 / 1356 MEDLINE  
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[PMID]:27996177
[Au] Autor:Yao PL; Chen L; Dobrzanski TP; Zhu B; Kang BH; Müller R; Gonzalez FJ; Peters JM
[Ad] Endereço:Department of Veterinary and Biomedical Sciences and The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania.
[Ti] Título:Peroxisome proliferator-activated receptor-ß/δ inhibits human neuroblastoma cell tumorigenesis by inducing p53- and SOX2-mediated cell differentiation.
[So] Source:Mol Carcinog;56(5):1472-1483, 2017 May.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuroblastoma is a common childhood cancer typically treated by inducing differentiation with retinoic acid (RA). Peroxisome proliferator-activated receptor-ß/δ, (PPARß/δ) is known to promote terminal differentiation of many cell types. In the present study, PPARß/δ was over-expressed in three human neuroblastoma cell lines, NGP, SK-N-BE(2), and IMR-32, that exhibit high, medium, and low sensitivity, respectively, to retinoic acid-induced differentiation to determine if PPARß/δ and retinoic acid receptors (RARs) could be jointly targeted to increase the efficacy of treatment. All-trans-RA (atRA) decreased expression of SRY (sex determining region Y)-box 2 (SOX2), a stem cell regulator and marker of de-differentiation, in NGP and SK-N-BE(2) cells with inactive or mutant tumor suppressor p53, respectively. However, atRA did not suppress SOX2 expression in IMR-32 cells carrying wild-type p53. Over-expression and/or ligand activation of PPARß/δ reduced the average volume and weight of ectopic tumor xenografts from NGP, SK-N-BE(2), or IMR-32 cells compared to controls. Compared with that found with atRA, PPARß/δ suppressed SOX2 expression in NGP and SK-N-BE(2) cells and ectopic xenografts, and was also effective in suppressing SOX2 expression in IMR-32 cells that exhibit higher p53 expression compared to the former cell lines. Combined, these observations demonstrate that activating or over-expressing PPARß/δ induces cell differentiation through p53- and SOX2-dependent signaling pathways in neuroblastoma cells and tumors. This suggests that combinatorial activation of both RARα and PPARß/δ may be suitable as an alternative therapeutic approach for RA-resistant neuroblastoma patients.
[Mh] Termos MeSH primário: Neuroblastoma/patologia
PPAR delta/metabolismo
PPAR beta/metabolismo
Fatores de Transcrição SOXB1/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/fisiologia
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos
Feminino
Seres Humanos
Camundongos Nus
Neuroblastoma/tratamento farmacológico
Neuroblastoma/metabolismo
PPAR delta/genética
PPAR beta/genética
PTEN Fosfo-Hidrolase/metabolismo
Receptor alfa de Ácido Retinoico/metabolismo
Tretinoína/farmacologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PPAR delta); 0 (PPAR-beta); 0 (Retinoic Acid Receptor alpha); 0 (SOX2 protein, human); 0 (SOXB1 Transcription Factors); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 5688UTC01R (Tretinoin); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170426
[Lr] Data última revisão:
170426
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22607



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