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Pesquisa : G05.308.203.374.790 [Categoria DeCS]
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[PMID]:29364956
[Au] Autor:Winzi M; Casas Vila N; Paszkowski-Rogacz M; Ding L; Noack S; Theis M; Butter F; Buchholz F
[Ad] Endereço:Medical Systems Biology, Faculty of Medicine Carl Gustav Carus, University Cancer Center, TU Dresden, Dresden, Germany.
[Ti] Título:The long noncoding RNA lncR492 inhibits neural differentiation of murine embryonic stem cells.
[So] Source:PLoS One;13(1):e0191682, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RNA interference (RNAi) screens have been shown to be valuable to study embryonic stem cell (ESC) self-renewal and they have been successfully applied to identify coding as well as noncoding genes required for maintaining pluripotency. Here, we used an RNAi library targeting >640 long noncoding RNAs (lncRNA) to probe for their role in early cell differentiation. Utilizing a Sox1-GFP ESC reporter cell line, we identified the lncRNA lncR492 as lineage-specific inhibitor of neuroectodermal differentiation. Molecular characterization showed that lncR492 interacts with the mRNA binding protein HuR and facilitates its inhibitory function by activation of Wnt signaling. Thus, lncRNAs modulate the fate decision of pluripotent stem cells.
[Mh] Termos MeSH primário: Diferenciação Celular
Células-Tronco Embrionárias/citologia
Neurônios/citologia
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Animais
Camundongos
Interferência de RNA
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Long Noncoding)
[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:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191682


  2 / 43408 MEDLINE  
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[PMID]:29267502
[Au] Autor:Liu C; Shui CL; Wang Q; Luo H; Gu CG
[Ad] Endereço:Department of Urology, The Second People's Hospital of Deyang City, Deyang, Sichuan Province, China.
[Ti] Título:Mechanism of hif-1α mediated hypoxia-induced permeability changes in bladder endothelial cells.
[So] Source:Braz J Med Biol Res;51(2):e6768, 2017 Dec 18.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:This study aimed to investigate the mechanism of hypoxia-inducible factor-1 alpha (HIF-1α) mediated hypoxia-induced permeability changes in bladder endothelial cells. Models of in vitro hypoxic cell culture of bladder cancer, bladder cancer cells with low HIF-1α expression and HIF-1α RNA interference (RNAi) expression vector were established. Western blot and reverse transcription polymerase chain reaction (RT-PCR) were used to detect the expression of HIF-1α and vascular endothelial growth factor (VEGF) in each group. Bladder cell permeability was determined. Results showed that protein and mRNA expression of HIF-1α and VEGF at 3 and 12 h of hypoxia were significantly higher than normal control (P<0.05), and peaked at 12 h. HIF-1α and VEGF expression in the hypoxic group and hypoxic+3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole (YC-1) group were significantly higher than normal control (P<0.05), while expression in the hypoxic+YC-1 group was significantly lower than the hypoxic group (P<0.05). Bladder cell permeability in the hypoxic and hypoxic+YC-1 group were significantly increased compared to normal control (P<0.05), while in the hypoxic+YC-1 group was significantly decreased compared to the hypoxic group (P<0.05). Most of the cells in the stably transfected HIF-1α RNAi expression vector pcDNA6.2-GW/EmGFP-miR-siHIF-1α expressed green fluorescence protein (GFP) under fluorescence microscope. pcDNA6.2-GW/EmGFP-miR-siHIF-1α could significantly inhibit HIF-1α gene expression (P<0.05). HIF-1α and VEGF expression in the hypoxic group and siHIF-1α hypoxic group were significantly higher than normal group (P<0.05), while expression in the siHIF-1α hypoxic group was significantly lower than the hypoxic group (P<0.05). Findings suggest that HIF-1α is an important factor in the increase of bladder cancer cell permeability.
[Mh] Termos MeSH primário: Células Endoteliais/fisiologia
Subunidade alfa do Fator 1 Induzível por Hipóxia/fisiologia
Hipóxia Tumoral/fisiologia
Neoplasias da Bexiga Urinária/metabolismo
Fator A de Crescimento do Endotélio Vascular/fisiologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular Tumoral
Células Endoteliais/patologia
Regulação Neoplásica da Expressão Gênica/fisiologia
Subunidade alfa do Fator 1 Induzível por Hipóxia/análise
Permeabilidade
Interferência de RNA
Coelhos
Reação em Cadeia da Polimerase em Tempo Real
Neoplasias da Bexiga Urinária/genética
Neoplasias da Bexiga Urinária/patologia
Fator A de Crescimento do Endotélio Vascular/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Vascular Endothelial Growth Factor A)
[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:171222
[St] Status:MEDLINE


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[PMID]:28461099
[Au] Autor:Alaaeldin E; Abu Lila AS; Ando H; Fukushima M; Huang CL; Wada H; Sarhan HA; Khaled KA; Ishida T
[Ad] Endereço:Department of Pharmacokinetics and Biopharmaceutics, Institute of Biomedical Sciences, Tokushima University, 1-78-1, Sho-machi, Tokushima 770-8505, Japan; Department of Pharmaceutics, Faculty of Pharmacy, Minia University, Minia 61519, Egypt.
[Ti] Título:Co-administration of liposomal l-OHP and PEGylated TS shRNA-lipoplex: A novel approach to enhance anti-tumor efficacy and reduce the immunogenic response to RNAi molecules.
[So] Source:J Control Release;255:210-217, 2017 Jun 10.
[Is] ISSN:1873-4995
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Many therapeutic strategies have been applied in efforts to conquer the development and/or progression of cancer. The combination of chemotherapy and an RNAi-based approach has proven to be an efficient anticancer therapy. However, the feasibility of such a therapeutic strategy has been substantially restricted either by the failure to achieve the efficient delivery of RNAi molecules to tumor tissue or by the immunostimulatory response triggered by RNAi molecules. In this study, therefore, we intended to investigate the efficacy of using liposomal oxaliplatin (liposomal l-OHP) to guarantee the efficient delivery of RNAi molecules, namely shRNA against thymidylate synthase (TS shRNA) complexed with cationic liposome (TS shRNA-lipoplex), to solid tumors, and to suppress the immunostimulatory effect of RNAi molecules, TS shRNA, following intravenous administration. Herein, we describe how liposomal l-OHP enhanced the intra-tumor accumulation of TS shRNA-lipoplex and significantly reduced the immunostimulatory response triggered by TS shRNA. Consequently, such enhanced accumulation of TS shRNA-lipoplex along with the cytotoxic effect of liposomal l-OHP led to a remarkable tumor growth suppression (compared to mono-therapy) following systemic administration. Our results, therefore, may have important implications for the provision of a safer and more applicable combination therapy of RNAi molecules and anti-cancer agents that can produce a more reliable anti-tumor effect.
[Mh] Termos MeSH primário: Antineoplásicos/administração & dosagem
Neoplasias/terapia
Compostos Organoplatínicos/administração & dosagem
RNA Interferente Pequeno/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Antineoplásicos/farmacocinética
Antineoplásicos/uso terapêutico
Linhagem Celular Tumoral
Citocinas/metabolismo
Seres Humanos
Lipossomos
Masculino
Camundongos Endogâmicos BALB C
Camundongos Nus
Neoplasias/genética
Neoplasias/metabolismo
Compostos Organoplatínicos/química
Compostos Organoplatínicos/farmacocinética
Compostos Organoplatínicos/uso terapêutico
Polietilenoglicóis/química
Interferência de RNA
RNA Interferente Pequeno/química
RNA Interferente Pequeno/farmacocinética
RNA Interferente Pequeno/uso terapêutico
Timidilato Sintase/genética
Distribuição Tecidual
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cytokines); 0 (Liposomes); 0 (Organoplatinum Compounds); 0 (RNA, Small Interfering); 04ZR38536J (oxaliplatin); 30IQX730WE (Polyethylene Glycols); EC 2.1.1.45 (Thymidylate Synthase)
[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


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[PMID]:29442029
[Au] Autor:Mu P; Zhou J; Ma X; Zhang G; Li Y
[Ti] Título:Expression, regulation and function of MicroRNAs in endometriosis.
[So] Source:Pharmazie;71(8):434-438, 2016 Aug 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Endometriosis (EMS), characterized by the presence and growth of functional en do met rial-like tissues outside the uterine cavity, is a common and benign gyneco logical disorder with a poorly understood and somewhat enigmatic etiopathogenesis and pathophysiology. MicroRNAs (miRNAs) are single-stranded 19-25 nucleotide-long RNAs and have an important role in post-transcriptional gene silencing by base pairing with target mRNAs. Recent research has shown that miRNAs and their target mRNAs are differentially expressed in endometriosis and other disorders of the female reproductive system. In this paper, we review the recent progress in understanding the roles of miRNAs in endometriosis, and specific miRNAs as biomarkers and therapeutic targets for endometriosis.
[Mh] Termos MeSH primário: Endometriose/genética
MicroRNAs/biossíntese
[Mh] Termos MeSH secundário: Biomarcadores
Endometriose/diagnóstico
Feminino
Regulação da Expressão Gênica
Seres Humanos
MicroRNAs/análise
MicroRNAs/genética
Interferência de RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (MicroRNAs)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.5904


  5 / 43408 MEDLINE  
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[PMID]:28922779
[Au] Autor:Hanley CJ; Mellone M; Ford K; Thirdborough SM; Mellows T; Frampton SJ; Smith DM; Harden E; Szyndralewiez C; Bullock M; Noble F; Moutasim KA; King EV; Vijayanand P; Mirnezami AH; Underwood TJ; Ottensmeier CH; Thomas GJ
[Ad] Endereço:Cancer Sciences Unit, University of Southampton Faculty of Medicine, Southampton, UK; Genkyotex SA, Plan-les-Ouates, Switzerland; La Jolla Institute for Allergy and Immunology, La Jolla, CA.
[Ti] Título:Targeting the Myofibroblastic Cancer-Associated Fibroblast Phenotype Through Inhibition of NOX4.
[So] Source:J Natl Cancer Inst;110(1), 2018 Jan 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Cancer-associated fibroblasts (CAFs) are tumor-promoting and correlate with poor survival in many cancers, which has led to their emergence as potential therapeutic targets. However, effective methods to manipulate these cells clinically have yet to be developed. Methods: CAF accumulation and prognostic significance in head and neck cancer (oral, n = 260; oropharyngeal, n = 271), and colorectal cancer (n = 56) was analyzed using immunohistochemistry. Mechanisms regulating fibroblast-to-myofibroblast transdifferentiation were investigated in vitro using RNA interference/pharmacological inhibitors followed by polymerase chain reaction (PCR), immunoblotting, immunofluorescence, and functional assays. RNA sequencing/bioinformatics and immunohistochemistry were used to analyze NAD(P)H Oxidase-4 (NOX4) expression in different human tumors. NOX4's role in CAF-mediated tumor progression was assessed in vitro, using CAFs from multiple tissues in Transwell and organotypic culture assays, and in vivo, using xenograft (n = 9-15 per group) and isograft (n = 6 per group) tumor models. All statistical tests were two-sided. Results: Patients with moderate/high levels of myofibroblastic-CAF had a statistically significant decrease in cancer-specific survival rates in each cancer type analyzed (hazard ratios [HRs] = 1.69-7.25, 95% confidence intervals [CIs] = 1.11 to 31.30, log-rank P ≤ .01). Fibroblast-to-myofibroblast transdifferentiation was dependent on a delayed phase of intracellular reactive oxygen species, generated by NOX4, across different anatomical sites and differentiation stimuli. A statistically significant upregulation of NOX4 expression was found in multiple human cancers (P < .001), strongly correlating with myofibroblastic-CAFs (r = 0.65-0.91, adjusted P < .001). Genetic/pharmacological inhibition of NOX4 was found to revert the myofibroblastic-CAF phenotype ex vivo (54.3% decrease in α-smooth muscle actin [α-SMA], 95% CI = 10.6% to 80.9%, P = .009), prevent myofibroblastic-CAF accumulation in vivo (53.2%-79.0% decrease in α-SMA across different models, P ≤ .02) and slow tumor growth (30.6%-64.0% decrease across different models, P ≤ .04). Conclusions: These data suggest that pharmacological inhibition of NOX4 may have broad applicability for stromal targeting across cancer types.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Fibroblastos Associados a Câncer/patologia
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Carcinoma de Células Escamosas/tratamento farmacológico
Neoplasias Colorretais/química
Neoplasias Esofágicas/tratamento farmacológico
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Bucais/química
Miofibroblastos/patologia
NADPH Oxidases/antagonistas & inibidores
Neoplasias Orofaríngeas/química
[Mh] Termos MeSH secundário: Actinas/análise
Adenocarcinoma/química
Adenocarcinoma/genética
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Fibroblastos Associados a Câncer/química
Fibroblastos Associados a Câncer/fisiologia
Carcinoma Pulmonar de Células não Pequenas/química
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma de Células Escamosas/química
Carcinoma de Células Escamosas/genética
Contagem de Células
Transdiferenciação Celular/efeitos dos fármacos
Transdiferenciação Celular/genética
Neoplasias Colorretais/patologia
Progressão da Doença
Neoplasias Esofágicas/química
Neoplasias Esofágicas/genética
Feminino
Neoplasias de Cabeça e Pescoço/química
Neoplasias de Cabeça e Pescoço/tratamento farmacológico
Neoplasias de Cabeça e Pescoço/genética
Seres Humanos
Neoplasias Pulmonares/química
Neoplasias Pulmonares/genética
Masculino
Camundongos
Meia-Idade
Neoplasias Bucais/patologia
Miofibroblastos/química
NADPH Oxidase 4
NADPH Oxidases/análise
NADPH Oxidases/genética
Transplante de Neoplasias
Neoplasias Orofaríngeas/patologia
Fenótipo
Pirazóis/uso terapêutico
Piridinas/uso terapêutico
Interferência de RNA
Espécies Reativas de Oxigênio/metabolismo
Taxa de Sobrevida
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (GKT137831); 0 (Pyrazoles); 0 (Pyridines); 0 (Reactive Oxygen Species); EC 1.6.3.- (NADPH Oxidase 4); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.- (NOX4 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx121


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[PMID]:28453731
[Au] Autor:Demolli S; Doddaballapur A; Devraj K; Stark K; Manavski Y; Eckart A; Zehendner CM; Lucas T; Korff T; Hecker M; Massberg S; Liebner S; Kaluza D; Boon RA; Dimmeler S
[Ad] Endereço:Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe University, Theodor Stern Kai 7, 60590 Frankfurt, Germany.
[Ti] Título:Shear stress-regulated miR-27b controls pericyte recruitment by repressing SEMA6A and SEMA6D.
[So] Source:Cardiovasc Res;113(6):681-691, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: Vessel maturation involves the recruitment of mural cells such as pericytes and smooth muscle cells. Laminar shear stress is a major trigger for vessel maturation, but the molecular mechanisms by which shear stress affects recruitment of pericytes are unclear. MicroRNAs (miRs) are small non-coding RNAs, which post-transcriptionally control gene expression. The aim of the present study was to unveil the mechanism by which shear stress-regulated microRNAs contribute to vessel maturation. Methods and results: Here, we show that laminar shear stress increased miR-27a and miR-27b expression in vitro and in ex vivo in mouse femoral artery explants. Overexpression of miR-27b in endothelial cells increased pericyte adhesion and pericyte recruitment in vitro. In vitro barrier function of endothelial-pericyte co-cultures was augmented by miR-27b overexpression, whereas inhibition of miR-27a/b reduced adhesion and pericyte coverage and decreased barrier functions. In vivo, pharmacological inhibition of miR-27a/b by locked nucleic acid antisense oligonucleotides significantly reduced pericyte coverage and increased water content in the murine uterus. MiR-27b overexpression repressed semaphorins (SEMA), which mediate repulsive signals, and the vessel destabilizing human but not mouse Angiopoietin-2 (Ang-2). Silencing of SEMA6A and SEMA6D rescued the reduced pericyte adhesion by miR-27 inhibition. Furthermore, inhibition of SEMA6D increased barrier function of an endothelial-pericyte co-culture in vitro. Conclusion: The present study demonstrates for the first time that shear stress-regulated miR-27b promotes the interaction of endothelial cells with pericytes, partly by repressing SEMA6A and SEMA6D.
[Mh] Termos MeSH primário: Encéfalo/irrigação sanguínea
Comunicação Celular
Movimento Celular
Células Endoteliais/metabolismo
Mecanotransdução Celular
Microvasos/metabolismo
Pericitos/metabolismo
Semaforinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Técnicas de Cocultura
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
MicroRNAs/genética
MicroRNAs/metabolismo
Interferência de RNA
Semaforinas/genética
Estresse Mecânico
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN27 microRNA, human); 0 (MicroRNAs); 0 (Mirn27 microRNA, mouse); 0 (SEMA6A protein, human); 0 (Sema6a protein, mouse); 0 (Sema6d protein, mouse); 0 (Semaphorins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx032


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[PMID]:29295999
[Au] Autor:Han S; Ren Y; He W; Liu H; Zhi Z; Zhu X; Yang T; Rong Y; Ma B; Purwin TJ; Ouyang Z; Li C; Wang X; Wang X; Yang H; Zheng Y; Aplin AE; Liu J; Shao Y
[Ad] Endereço:Frontier Institute of Science and Technology, and Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, China.
[Ti] Título:ERK-mediated phosphorylation regulates SOX10 sumoylation and targets expression in mutant BRAF melanoma.
[So] Source:Nat Commun;9(1):28, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In human mutant BRAF melanoma cells, the stemness transcription factor FOXD3 is rapidly induced by inhibition of ERK1/2 signaling and mediates adaptive resistance to RAF inhibitors. However, the mechanism underlying ERK signaling control of FOXD3 expression remains unknown. Here we show that SOX10 is both necessary and sufficient for RAF inhibitor-induced expression of FOXD3 in mutant BRAF melanoma cells. SOX10 activates the transcription of FOXD3 by binding to a regulatory element in FOXD3 promoter. Phosphorylation of SOX10 by ERK inhibits its transcription activity toward multiple target genes by interfering with the sumoylation of SOX10 at K55, which is essential for its transcription activity. Finally, depletion of SOX10 sensitizes mutant BRAF melanoma cells to RAF inhibitors in vitro and in vivo. Thus, our work discovers a novel phosphorylation-dependent regulatory mechanism of SOX10 transcription activity and completes an ERK1/2/SOX10/FOXD3/ERBB3 axis that mediates adaptive resistance to RAF inhibitors in mutant BRAF melanoma cells.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica/genética
Melanoma/genética
Mutação
Proteínas Proto-Oncogênicas B-raf/genética
Fatores de Transcrição SOXE/genética
Neoplasias Cutâneas/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Inibidores Enzimáticos/farmacologia
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/metabolismo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Indóis/farmacologia
Melanoma/tratamento farmacológico
Melanoma/metabolismo
Camundongos Endogâmicos BALB C
Camundongos Nus
Fosforilação
Proteínas Proto-Oncogênicas B-raf/metabolismo
Interferência de RNA
Receptor ErbB-3/genética
Receptor ErbB-3/metabolismo
Fatores de Transcrição SOXE/metabolismo
Neoplasias Cutâneas/tratamento farmacológico
Neoplasias Cutâneas/metabolismo
Sulfonamidas/farmacologia
Sumoilação
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (FOXD3 protein, human); 0 (Forkhead Transcription Factors); 0 (Indoles); 0 (SOX10 protein, human); 0 (SOXE Transcription Factors); 0 (Sulfonamides); 207SMY3FQT (vemurafenib); EC 2.7.10.1 (ERBB3 protein, human); EC 2.7.10.1 (Receptor, ErbB-3); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02354-x


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[PMID]:29295976
[Au] Autor:Liu CY; Zhang YH; Li RB; Zhou LY; An T; Zhang RC; Zhai M; Huang Y; Yan KW; Dong YH; Ponnusamy M; Shan C; Xu S; Wang Q; Zhang YH; Zhang J; Wang K
[Ad] Endereço:Center for Developmental Cardiology, Institute for Translational Medicine, College of Medicine, Qingdao University, Qingdao, 266021, China.
[Ti] Título:LncRNA CAIF inhibits autophagy and attenuates myocardial infarction by blocking p53-mediated myocardin transcription.
[So] Source:Nat Commun;9(1):29, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Increasing evidence suggests that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes. However, little is known about the effects of lncRNAs on autophagy. Here we report that a lncRNA, termed cardiac autophagy inhibitory factor (CAIF), suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53-mediated myocardin transcription. Myocardin expression is upregulated upon H O and ischemia/reperfusion, and knockdown of myocardin inhibits autophagy and attenuates myocardial infarction. p53 regulates cardiomyocytes autophagy and myocardial ischemia/reperfusion injury by regulating myocardin expression. CAIF directly binds to p53 protein and blocks p53-mediated myocardin transcription, which results in the decrease of myocardin expression. Collectively, our data reveal a novel CAIF-p53-myocardin axis as a critical regulator in cardiomyocyte autophagy, which will be potential therapeutic targets in treatment of defective autophagy-associated cardiovascular diseases.
[Mh] Termos MeSH primário: Autofagia/genética
Infarto do Miocárdio/genética
Proteínas Nucleares/genética
RNA Longo não Codificante/genética
Transativadores/genética
Ativação Transcricional
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Células Cultivadas
Camundongos
Infarto do Miocárdio/patologia
Traumatismo por Reperfusão Miocárdica/genética
Traumatismo por Reperfusão Miocárdica/metabolismo
Miócitos Cardíacos/metabolismo
Proteínas Nucleares/metabolismo
Ligação Proteica
Interferência de RNA
RNA Longo não Codificante/metabolismo
Transativadores/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nuclear Proteins); 0 (RNA, Long Noncoding); 0 (Trans-Activators); 0 (Tumor Suppressor Protein p53); 0 (myocardin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02280-y


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[PMID]:29190611
[Au] Autor:Liu J; Rao J; Lou X; Zhai J; Ni Z; Wang X
[Ad] Endereço:Department of Respiratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
[Ti] Título:Upregulated TRIM11 Exerts its Oncogenic Effects in Hepatocellular Carcinoma Through Inhibition of P53.
[So] Source:Cell Physiol Biochem;44(1):255-266, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The tripartite motif containing (TRIM) family plays crucial roles in tumor development and progression. However, little is known about the function and mechanism of TRIM11 in hepatocellular carcinoma (HCC). METHODS: The expression levels of TRIM11 were examined by real-time PCR, Western blot and Immunohistochemical (IHC) staining. TRIM11 knockdown cells were produced by lentivirus infection, and functional assays, such as MTT, colony formation assay, migration and invasion assays and a xenograft tumor model were used to investigate the role of TRIM11 in HCC. We also determined the effect of TRIM11 on p53 signaling and its downstream molecules. RESULTS: We found that TRIM11 mRNA and protein levels were significantly increased in HCC tissues as compared with normal tissues; increased levels correlated with poor patient survival. By loss- and gain-of-function investigations, knockdown of TRIM11 suppressed cell proliferation, migration, invasion in vitro and tumor growth in vivo. Moreover, TRIM11 negatively regulated p53 expression. Knockdown of p53 abrogated the in vitro and in vivo biological functions of TRIM11 shRNA in HCC cells. CONCLUSIONS: These data show that TRIM11 exerts its oncogenic effect in HCC by downregulating p53 both in vitro and in vivo. Our data provide new insights into the pathogenesis of HCC and indicate that TRIM11 may serve as a new therapeutic target for HCC treatment.
[Mh] Termos MeSH primário: Proteínas com Motivo Tripartido/genética
Proteínas com Motivo Tripartido/metabolismo
Proteína Supressora de Tumor p53/metabolismo
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Movimento Celular
Proliferação Celular
Ciclina D1/genética
Ciclina D1/metabolismo
Inibidor de Quinase Dependente de Ciclina p21/genética
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Inibidor de Quinase Dependente de Ciclina p27/genética
Inibidor de Quinase Dependente de Ciclina p27/metabolismo
Regulação para Baixo
Transição Epitelial-Mesenquimal
Células Hep G2
Seres Humanos
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Transplante Heterólogo
Proteínas com Motivo Tripartido/antagonistas & inibidores
Proteína Supressora de Tumor p53/antagonistas & inibidores
Proteína Supressora de Tumor p53/genética
Ubiquitina-Proteína Ligases/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (RNA, Small Interfering); 0 (TP53 protein, human); 0 (Tripartite Motif Proteins); 0 (Tumor Suppressor Protein p53); 136601-57-5 (Cyclin D1); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); EC 2.3.2.27 (TRIM11 protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1159/000484678


  10 / 43408 MEDLINE  
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[PMID]:28464292
[Au] Autor:Charbgoo F; Behmanesh M; Nikkhah M; Kane EG
[Ad] Endereço:Department of Nanobiotechnology, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
[Ti] Título:RNAi mediated gene silencing of ITPA using a targeted nanocarrier: Apoptosis induction in SKBR3 cancer cells.
[So] Source:Clin Exp Pharmacol Physiol;44(8):888-894, 2017 Aug.
[Is] ISSN:1440-1681
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:A pure nucleotide pool is required for high-fidelity DNA replication and prevention of carcinogenesis in living cells. Human inosine triphosphatase (ITPase), encoded by the ITPA gene, plays a critical role in maintaining the purity of the cellular nucleotide pool by excluding nucleotides that enhance mutagenesis. ITPase is a nucleoside triphosphate pyrophosphatase that hydrolyzes the non-canonical nucleotides inosine triphosphate (ITP) and xanthine triphosphate (XTP). The monophosphate products of ITPase reactions are subsequently excluded from the nucleotide pool and the improper substitution of ITP and XTP into DNA and RNA is prevented. Previous studies show that deficiency in ITPA can suppress cellular growth and enhance DNA instability. In this study, we evaluated the influence of effective ITPA down-regulation on the induction of apoptosis in a human cancer cell line using folate-single wall nanotubes (SWNT) as a targeted nanocarrier. We assessed whether SWNT enhances IPTA-siRNA transfection efficiency in cancer cells using folate as a homing device. Since folate receptor is considerably overexpressed in cancer cells, conjugation of SWNTs to folate could enhance their cancer-specific penetrance. We found that nanocarrier mediated ITPA-siRNA transfection into SKBR3 cells caused significant reduction of ITPA mRNA expression level and complete down-regulation of the ITPase protein product. The silencing of ITPA led to promotion of apoptosis in SWNT-treated SKBR3 cancer cells.
[Mh] Termos MeSH primário: Apoptose/genética
Portadores de Fármacos/química
Nanoestruturas/química
Nanotubos de Carbono/química
Pirofosfatases/deficiência
Pirofosfatases/genética
Interferência de RNA
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Regulação para Baixo/genética
Ácido Fólico/química
Seres Humanos
Hidrólise
RNA Interferente Pequeno/química
RNA Interferente Pequeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Carriers); 0 (Nanotubes, Carbon); 0 (RNA, Small Interfering); 935E97BOY8 (Folic Acid); EC 3.6.1.- (Pyrophosphatases); EC 3.6.1.19 (ITPA protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/1440-1681.12776



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