Base de dados : MEDLINE
Pesquisa : G04.198 [Categoria DeCS]
Referências encontradas : 96604 [refinar]
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[PMID]:29366479
[Au] Autor:Xia E; Bhandari A; Shen Y; Zhou X; Sindan N; Xiang J; Guan Y; Yang F; Wang O
[Ad] Endereço:Department of Thyroid & Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, PR China.
[Ti] Título:LncRNA CCND2-AS1 promotes proliferation, migration, and invasion in papillary thyroid carcinoma.
[So] Source:Biochem Biophys Res Commun;496(2):628-632, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In decades, a lot of long non-coding RNAs (LncRNAs) have been proven to exert influences on tumorigenesis in vitro and in vivo. Many lncRNAs have been reported as effective therapeutic targets and biomarkers in various cancers. However, whether LncRNAs are associated with the progression of PTC remains largely unknown. In this study, we measured the expression of CCND2-AS1 in PTC cell lines by quantitative real-time polymerase chain reaction (qRT-PCR).We found that CCND2-AS1 expression was significantly over-expressed in PTC cell lines compared to normal thyroid epithelial cells. Gain-and loss-of-function experiments were performed to investigate the role of CCND2-AS1 in PTC cells. In vitro experiments, we proved that CCND2-AS1 knockdown in TPC1 significantly suppressed cell proliferation, migration, and invasion, while CCND2-AS1 overexpression in BCPAP had the opposite effects. Meanwhile, we also found that CCND2-AS1 could regulate N-cadherin and Vimentin expression, which may influence invasion and migration. Our findings indicate that the lncRNA CCND2-AS1 is a gene associated with PTC and might become a potential therapeutic target.
[Mh] Termos MeSH primário: Carcinoma Papilar/genética
Regulação Neoplásica da Expressão Gênica
Invasividade Neoplásica/genética
RNA Longo não Codificante/genética
Neoplasias da Glândula Tireoide/genética
[Mh] Termos MeSH secundário: Carcinoma Papilar/patologia
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Seres Humanos
Invasividade Neoplásica/patologia
Glândula Tireoide/patologia
Neoplasias da Glândula Tireoide/patologia
[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:180126
[St] Status:MEDLINE


  2 / 96604 MEDLINE  
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[PMID]:28456536
[Au] Autor:More Bayona JA; Karuppannan AK; Barreda DR
[Ad] Endereço:Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2P5, Canada.
[Ti] Título:Contribution of leukocytes to the induction and resolution of the acute inflammatory response in chickens.
[So] Source:Dev Comp Immunol;74:167-177, 2017 Sep.
[Is] ISSN:1879-0089
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A successful immune response against invading pathogens relies on the efficient activation of host defense mechanisms and a timely return to immune homeostasis. Despite their importance, these mechanisms remain ill-defined in most animal groups. This study focuses on the acute inflammatory response of chickens, important both as an avian model with a unique position in evolution as well as an increasingly notable target of infectious zoonotic diseases. We took advantage of an in vivo self-resolving intra-abdominal challenge model to provide an integrative view of leukocyte responses during the induction and resolution phases of acute inflammation. Our results showed rapid leukocyte infiltration into the abdominal cavity post zymosan challenge (significant increase as early as 4 h), which was dominated by heterophils. Peak leukocyte infiltration and ROS production reached maximum levels at 12 h post challenge, which was significantly earlier than comparative studies in teleost fish and mice. Both heterophils and monocyte/macrophages contributed to ROS production. Local leukocyte infiltration was preceded by an increase in peripheral leukocytes and a drop in the number of bone marrow leukocytes. The proportion of apoptotic leukocytes increased following peak of acute inflammation, rising to significant levels within the abdominal cavity by 48 h, consistent with other indicators for the resolution of inflammation. Importantly, comparison of chicken phagocytic responses with those previously shown in agnathan, teleost and murine models suggested a progressive evolutionary shift towards an increased sensitivity to pro-inflammatory pathogen-derived particles and decreased sensitivity towards homeostatic stimuli. Thus, while significant conservation can be noted across the immune systems of endotherms, this study highlights additional unique features that govern the induction and resolution of acute inflammation in the avian system, which may be relevant to disease susceptibility and performance.
[Mh] Termos MeSH primário: Doenças das Aves/imunologia
Galinhas/imunologia
Inflamação/imunologia
Leucócitos/imunologia
Peritônio/fisiologia
Zoonoses/imunologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Apoptose
Evolução Biológica
Movimento Celular
Proliferação Celular
Peixes
Seres Humanos
Imunidade Inata
Camundongos
Fagocitose
Fisiologia Comparada
Espécies Reativas de Oxigênio/metabolismo
Zimosan/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 9010-72-4 (Zymosan)
[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:170501
[St] Status:MEDLINE


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[PMID]:28452702
[Au] Autor:Shin JM; Kang JH; Lee SA; Park IH; Lee HM
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Seoul, South Korea.
[Ti] Título:Effect of doxycycline on epithelial-mesenchymal transition the p38/Smad pathway in respiratory epithelial cells.
[So] Source:Am J Rhinol Allergy;31(2):71-77, 2017 Mar 01.
[Is] ISSN:1945-8932
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Doxycycline has antibacterial and anti-inflammatory effects, and it also suppresses collagen biosynthesis. This study aimed to confirm the effects and mechanism of doxycycline on transforming growth factor (TGF) beta 1 induced epithelial-mesenchymal transition and cell migration in A549 and primary nasal epithelial cells. METHODS: A 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay and phalloidin-fluorescein isothiocyanate staining were used to evaluate cytotoxicity and cellular morphologic changes. Western blot and immunofluorescence staining were used to determine the expression levels of E-cadherin, vimentin, alpha-smooth muscle actin, fibronectin, phosphorylated Smad2/3, and mitogen-activated protein kinases. Scratch and transwell migration assays were used to assess cellular migration ability. RESULTS: Doxycycline (0-10 µg/mL) had no significant cytotoxic effects in A549 and primary nasal epithelial cells. Increased expression of mesenchymal markers, including vimentin, alpha-smooth muscle actin, and fibronectin in TGF beta 1 induced A549 cells were downregulated by doxycycline treatment. In contrast, E-cadherin expression was upregulated in TGF beta 1 induced A549 cells. An in vitro cell migration assay showed that doxycycline also inhibited the ability of TGF beta 1 induced migration. Doxycycline treatment suppressed the activation of Smad2/3 and p38, whereas its inhibitory effects were similar to each element-specific inhibitor in A549 and primary nasal epithelial cells. CONCLUSION: Doxycycline inhibited TGF beta 1 induced epithelial-to-mesenchymal transition and migration by targeting Smad2/3 and p38 signal pathways in respiratory epithelial cells.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Doxiciclina/farmacologia
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Mucosa Respiratória/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células A549
Caderinas/metabolismo
Movimento Celular/efeitos dos fármacos
Regulação da Expressão Gênica
Seres Humanos
Sistema de Sinalização das MAP Quinases
Cultura Primária de Células
Mucosa Respiratória/patologia
Proteína Smad2/metabolismo
Proteína Smad3/metabolismo
Fator de Crescimento Transformador beta/metabolismo
Vimentina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cadherins); 0 (Smad2 Protein); 0 (Smad3 Protein); 0 (Transforming Growth Factor beta); 0 (Vimentin); N12000U13O (Doxycycline)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.2500/ajra.2017.31.4410


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[PMID]:29270670
[Au] Autor:Lv C; Wang H; Tong Y; Yin H; Wang D; Yan Z; Liang Y; Wu D; Su Q
[Ad] Endereço:Department of General Surgery, Shengjing Hospital Affiliated to China Medical University, Shenyang City, Liaoning Province, 110004, People's Republic of China.
[Ti] Título:The function of BTG3 in colorectal cancer cells and its possible signaling pathway.
[So] Source:J Cancer Res Clin Oncol;144(2):295-308, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: B-cell translocation gene 3 (BTG3) has been identified as a candidate driver gene for various cancers, but its specific role in colorectal cancer (CRC) is poorly understood. We aimed to investigate the relationship between expression of BTG3 and clinicopathological features and prognosis, as well as to explore the effects and the role of a possible BTG3 molecular mechanism on aggressive colorectal cancer behavior. METHODS: BTG3 expression was assessed by immunohistochemistry (IHC) on specimens from 140 patients with CRC. The association of BTG3 expression with clinicopathological features was examined. To confirm the biological role of BTG3 in CRC, two CRC cell lines expressing BTG3 were used and BTG3 expression was knocked down by shRNA. CCK-8, cell cycle, apoptosis, migration, and invasion assays were performed. The influence of BTG3 knockdown was further investigated by genomic microarray to uncover the potential molecular mechanisms underlying BTG3-mediated CRC development and progression. RESULTS: BTG3 was downregulated in colorectal cancer tissues and positively correlated with pathological classification (p = 0.037), depth of invasion (p = 0.016), distant metastasis (p = 0.024), TNM stage (p = 0.007), and overall survival (OS) and disease-free survival (DFS). BTG3 knockdown promoted cell proliferation, migration, invasion, relieved G2 arrest, and inhibited apoptosis in HCT116 and LoVo cells. A genomic microarray analysis showed that numerous tumor-associated signaling pathways and oncogenes were altered by BTG3 knockdown. At the mRNA level, nine genes referred to the extracellular-regulated kinase/mitogen-activated protein kinase pathway were differentially expressed. Western blotting revealed that BTG3 knockdown upregulated PAK2, RPS6KA5, YWHAB, and signal transducer and activator of transcription (STAT)3 protein levels, but downregulated RAP1A, DUSP6, and STAT1 protein expression, which was consistent with the genomic microarray data. CONCLUSIONS: BTG3 expression might contribute to CRC carcinogenesis. BTG3 knockdown might strengthen the aggressive colorectal cancer behavior.
[Mh] Termos MeSH primário: Neoplasias Colorretais/metabolismo
Proteínas/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Movimento Celular/fisiologia
Proliferação Celular/fisiologia
Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Regulação para Baixo
Feminino
Técnicas de Silenciamento de Genes
Células HCT116
Células HT29
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Inclusão em Parafina
Proteínas/genética
Transdução de Sinais
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BTG3 protein, human); 0 (Proteins)
[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:171223
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2561-9


  5 / 96604 MEDLINE  
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[PMID]:29442033
[Au] Autor:Xia M; Wei J; Tong K
[Ti] Título:MiR-224 promotes proliferation and migration of gastric cancer cells through targeting PAK4.
[So] Source:Pharmazie;71(8):460-464, 2016 Aug 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Although recent studies have shown the important role and overexpression of miR-224 in several tumors, its function in gastric cancer has not yet been defined. In the present study, we tried to confirm the result of microRNAs microarray and further investigated the functions of miR-224 in gastric cancer, and tried to find new downstream targets of miR-224. In this study, the level of miR-224 was measured in gastric cancer cells with the normal human gastric epithelial cell. The effects of miR-224 of on proliferation, migration, and target protein expression were evaluated by CCK8 assay, colony assay, transwell migration assay, western blotting. In addition, luciferase reporter plasmid was constructed to demonstrate the direct target of miR-224. Overexpression of miR-224 was detected in the gastric cancer cells, especially in SCG-7901. Exogenous miR-224 expression promoted the proliferation and migration of gastric cells and abrogating expression of miR-224 suppressed proliferation, and migration of SCG-7901 cells in vitro. Luciferase assays revealed that miR-224 directly targeted the 3'UTR of p21-activated kinase 4 (PAK4). The present study provides an experimental foundation for miR-224 as a potential tumor suppressor that may decrease PAK4 expression to inhibit gastric cancer cells and that in the future, targeting of this miRNA may provide a novel strategy for the diagnosis and treatment of patients with this lethal disease.
[Mh] Termos MeSH primário: Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
MicroRNAs/uso terapêutico
Neoplasias Gástricas/patologia
Quinases Ativadas por p21/efeitos dos fármacos
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Células Epiteliais/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica
Genes Reporter/genética
Seres Humanos
MicroRNAs/genética
MicroRNAs/farmacologia
Plasmídeos/genética
Regulação para Cima
Cicatrização/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN224 microRNA, human); 0 (MicroRNAs); EC 2.7.1.11 (PAK4 protein, human); EC 2.7.11.1 (p21-Activated Kinases)
[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.2016.6580


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[PMID]:28469562
[Au] Autor:Di Bonito M; Studer M
[Ad] Endereço:Université Côte d'Azur, CNRS, Inserm, iBVNice, France.
[Ti] Título:Cellular and Molecular Underpinnings of Neuronal Assembly in the Central Auditory System during Mouse Development.
[So] Source:Front Neural Circuits;11:18, 2017.
[Is] ISSN:1662-5110
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:During development, the organization of the auditory system into distinct functional subcircuits depends on the spatially and temporally ordered sequence of neuronal specification, differentiation, migration and connectivity. Regional patterning along the antero-posterior axis and neuronal subtype specification along the dorso-ventral axis intersect to determine proper neuronal fate and assembly of rhombomere-specific auditory subcircuits. By taking advantage of the increasing number of transgenic mouse lines, recent studies have expanded the knowledge of developmental mechanisms involved in the formation and refinement of the auditory system. Here, we summarize several findings dealing with the molecular and cellular mechanisms that underlie the assembly of central auditory subcircuits during mouse development, focusing primarily on the rhombomeric and dorso-ventral origin of auditory nuclei and their associated molecular genetic pathways.
[Mh] Termos MeSH primário: Vias Auditivas
Regulação da Expressão Gênica no Desenvolvimento/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Animais
Vias Auditivas/citologia
Vias Auditivas/embriologia
Vias Auditivas/crescimento & desenvolvimento
Diferenciação Celular
Movimento Celular
Camundongos
Neurônios/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[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:170505
[St] Status:MEDLINE
[do] DOI:10.3389/fncir.2017.00018


  7 / 96604 MEDLINE  
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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


  8 / 96604 MEDLINE  
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[PMID]:28452328
[Au] Autor:Golafshan N; Gharibi H; Kharaziha M; Fathi M
[Ad] Endereço:Department of Materials Engineering, Isfahan University of Technology, Isfahan 84156-83111, Iran.
[Ti] Título:A facile one-step strategy for development of a double network fibrous scaffold for nerve tissue engineering.
[So] Source:Biofabrication;9(2):025008, 2017 04 28.
[Is] ISSN:1758-5090
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to develop a novel double network scaffold composed of polycaprolactone fumarate (PCLF) and eggshell membrane (ESM) (ESM:PCLF) by using the vacuum infiltration method. Compared to ESM, the mechanical properties of double network scaffold were significantly improved, depending on the solvents applied for double network scaffold formation; acetic acid and dichloromethane. Noticeably, the toughness and strength of double network scaffold prepared using acetic acid were significantly improved compared to ESM (26.6 and 25 times, respectively) attributed to the existence of hydrophilic functional groups in acetic acid which made ESM flexible to absorb further PCLF solution. To assess the effect of double network formation on the biological behavior of ESM, the attachment, proliferation and spreading of PC12 cells cultured on the ESM:PCLF scaffolds were evaluated. Results revealed that the number of cells attached on double network ESM:PCLF scaffold were nearly similar to ESM and significantly higher than that of on the tissue culture plate (2.6 times) and PCLF film (1.7 times). It is envisioned that the offered ESM:PCLF double network scaffold might have great potential to develop the constructs for nerve regeneration.
[Mh] Termos MeSH primário: Tecido Nervoso/fisiologia
Engenharia Tecidual
Tecidos Suporte/química
[Mh] Termos MeSH secundário: Animais
Materiais Biocompatíveis/síntese química
Materiais Biocompatíveis/química
Materiais Biocompatíveis/farmacologia
Membrana Celular/química
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Casca de Ovo
Interações Hidrofóbicas e Hidrofílicas
Microscopia Eletrônica de Varredura
Regeneração Nervosa/efeitos dos fármacos
Células PC12
Poliésteres/química
Ratos
Espectroscopia de Infravermelho com Transformada de Fourier
Raios Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Polyesters); 0 (poly(caprolactone fumarate))
[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:10.1088/1758-5090/aa68ed


  9 / 96604 MEDLINE  
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[PMID]:29237533
[Au] Autor:Wang J; Wang F; Gui YH
[Ad] Endereço:Department of Cardiovascular Medicine, Children's Hospital of Fudan University, Shanghai 200023, China. yhgui@shmu.edu.cn.
[Ti] Título:[Research advances in the mechanism of congenital heart disease induced by pregestational diabetes mellitus].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(12):1297-1300, 2017 Dec.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Congenital heart disease (CHD) is the most common birth defect at present and has a complex etiology which involves the combined effect of genetic and environmental factors. Pregestational diabetes mellitus is significantly associated with the development of CHD, but the detailed mechanism remains unknown. This article reviews the research advances in the molecular mechanism of CHD caused by pregestational diabetes mellitus.
[Mh] Termos MeSH primário: Cardiopatias Congênitas/etiologia
Gravidez em Diabéticas
[Mh] Termos MeSH secundário: Animais
Apoptose
Movimento Celular
Feminino
Seres Humanos
Crista Neural/fisiologia
Gravidez
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Reactive Oxygen Species)
[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:171215
[St] Status:MEDLINE


  10 / 96604 MEDLINE  
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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



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