Base de dados : MEDLINE
Pesquisa : D13.150.480.645 [Categoria DeCS]
Referências encontradas : 393 [refinar]
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[PMID]:28723693
[Au] Autor:Xu K; Liu P; Zhao Y
[Ad] Endereço:Department of Anesthesiology, Changchun, China.
[Ti] Título:Upregulation of microRNA-876 Induces Endothelial Cell Apoptosis by Suppressing Bcl-Xl in Development of Atherosclerosis.
[So] Source:Cell Physiol Biochem;42(4):1540-1549, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The injury and apoptotic cell death of endothelial cells hallmark the development of atherosclerosis (AS), characterized by dysregulation of lipid homeostasis, immune responses, and formation of coronary plaques. However, the mechanisms underlying the initiation of endothelial cell apoptosis remain ill-defined. Recent evidence suggests a role of microRNAs in the processes of AS-associated endothelial cell apoptosis. Thus, we studied this question in the current study. METHODS: AS was developed in ApoE (-/-) mice suppled with high-fat diet (HFD), compared to ApoE (-/-) mice suppled with normal diet (ND). Mouse endothelial cells were isolated from the aortic arch using flow cytometry based on their expression of Pecam-1. Oxidized low-density lipoprotein (ox-LDL) were used to treat human aortic endothelial cells (HAECs) as an in vitro model for AS. Gene expression was quantified by RT-qPCR and protein levels were analyzed by Western blotting. Apoptosis was evaluated by FITC Annexin V Apoptosis essay and by TUNEL staining. Prediction of the binding between miRNAs and 3'-UTR of mRNA from the target gene was performed by bioinformatics analyses and confirmed by a dual luciferase reporter assay. RESULTS: HFD mice, but not ND mice, developed AS in 12 weeks. Significantly reduced endothelial cell marks and significantly increased mesenchymal cell marks were detected in the aortic arch of the HFD mice, compared to the ND mice. The endothelial cell apoptosis was significantly higher in HFD mice, seemingly due to functional suppression of protein translation of anti-apoptotic Bcl-Xl protein through upregulation of miR-876. Similar results were obtained from in vitro study. Inhibition of miR-876 abolished the effects of ox-LDL-induced apoptotic cell death of HAECs. CONCLUSION: AS-associated endothelial cell apoptosis may partially result from downregulation of Bcl-Xl, through upregulation of miR-876 that binds and suppresses translation of Bcl-Xl mRNA.
[Mh] Termos MeSH primário: Aorta/metabolismo
Aterosclerose/genética
Células Endoteliais/metabolismo
Regulação da Expressão Gênica
MicroRNAs/genética
Proteína bcl-X/genética
[Mh] Termos MeSH secundário: Animais
Aorta/efeitos dos fármacos
Aorta/patologia
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Apoptose/genética
Aterosclerose/etiologia
Aterosclerose/metabolismo
Aterosclerose/patologia
Sítios de Ligação
Linhagem Celular
Dieta Hiperlipídica/efeitos adversos
Modelos Animais de Doenças
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/patologia
Seres Humanos
Lipoproteínas LDL/farmacologia
Camundongos
Camundongos Knockout
MicroRNAs/antagonistas & inibidores
MicroRNAs/metabolismo
Oligorribonucleotídeos Antissenso/genética
Oligorribonucleotídeos Antissenso/metabolismo
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Cultura Primária de Células
Biossíntese de Proteínas
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Transdução de Sinais
Proteína bcl-X/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Bcl2l1 protein, mouse); 0 (Lipoproteins, LDL); 0 (MicroRNAs); 0 (Oligoribonucleotides, Antisense); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (RNA, Messenger); 0 (bcl-X Protein); 0 (oxidized low density lipoprotein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1159/000479271


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[PMID]:28719898
[Au] Autor:Lin X; Zhen X; Huang H; Wu H; You Y; Guo P; Gu X; Yang F
[Ti] Título:Role of MiR-155 Signal Pathway in Regulating Podocyte Injury Induced by TGF-ß1.
[So] Source:Cell Physiol Biochem;42(4):1469-1480, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Transforming growth factor beta 1 (TGF-ß1) plays a critical role in the pathogenesis of glomerulosclerosis. The purpose of this study was to examine the effects of inhibition of miR-155 on podocyte injury induced by TGF-ß1 and to determine further molecular mediators involved in the effects of miR-155. METHODS: Conditionally immortalized podocytes were cultured in vitro and they were divided into four groups: control; TGF-ß1 treatment; TGF-ß1 with miR-155 knockdown [using antisense oligonucleotides against miR-155 (ASO-miR-155)] and TGF-ß1 with negative control antisense oligonucleotides (ASO-NC). Real time RT-PCR and Western blot analysis were employed to determine the mRNA and protein expression of nephrin, desmin and caspase-9, respectively. Flow cytometry was used to examine the apoptotic rate of podocytes and DAPI fluorescent staining was used to determine apoptotic morphology. In addition, we examined the levels of miR-155, TGF-ß1, nephrin, desmin and caspase-9 in glomerular tissues of nephropathy induced by intravenous injections of adriamycin in rats. RESULTS: mRNA and protein expression of desmin and caspase-9 was increased in cultured TGF-ß1-treated podocytes, whereas nephrin was decreased as compared with the control group. Importantly, miR-155 knockdown significantly attenuated upregulation of desmin and caspase-9, and alleviated impairment of nephrin induced by TGF-ß1. Moreover, the number of apoptotic podocytes was increased after exposure to TGF-ß1 and this was alleviated after miR-155 knockdown. Knocking down miR-155 also decreased an apoptosis rate of TGF-ß1-treated podocytes. Note that negative control antisense oligonucleotides failed to alter an increase of the apoptosis rate in TGF-ß1-treated podocytes. Consistent with in vitro results, expression of miR-155, TGF-ß1, desmin and caspase-9 was increased and nephrin was decreased in glomerular tissues with nephropathy in vivo experiments. CONCLUSIONS: TGF-ß1 impairs the protein expression of nephrin and amplifies the protein expression of desmin and caspase -9 via miR-155 signal pathway. Inhibition of miR-155 alleviates these changes in podocytes-treated with TGF-ß1 and attenuated apoptosis of podocytes. Our data suggest that miR-155 plays a role in mediating TGF-ß1-induced podocyte injury via nephrin, desmin and caspase-9. Results of the current study also indicate that blocking miR-155 signal has a protective effect on podocyte injury. Targeting one or more of these signaling molecules may present new opportunities for treatment and management of podocyte injury observed in glomerulosclerosis.
[Mh] Termos MeSH primário: Caspase 9/genética
Desmina/genética
Glomerulosclerose Segmentar e Focal/genética
Proteínas de Membrana/genética
MicroRNAs/genética
Podócitos/efeitos dos fármacos
Fator de Crescimento Transformador beta1/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Apoptose/genética
Caspase 9/metabolismo
Linhagem Celular Transformada
Desmina/metabolismo
Doxorrubicina
Regulação da Expressão Gênica
Glomerulosclerose Segmentar e Focal/induzido quimicamente
Glomerulosclerose Segmentar e Focal/metabolismo
Glomerulosclerose Segmentar e Focal/patologia
Masculino
Proteínas de Membrana/metabolismo
MicroRNAs/antagonistas & inibidores
MicroRNAs/metabolismo
Oligorribonucleotídeos Antissenso/genética
Oligorribonucleotídeos Antissenso/metabolismo
Podócitos/metabolismo
Podócitos/patologia
Ratos
Ratos Sprague-Dawley
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Desmin); 0 (MIRN155 microRNA, rat); 0 (Membrane Proteins); 0 (MicroRNAs); 0 (Oligoribonucleotides, Antisense); 0 (Transforming Growth Factor beta1); 0 (nephrin); 80168379AG (Doxorubicin); EC 3.4.22.- (Casp9 protein, rat); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1159/000479211


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[PMID]:28337887
[Au] Autor:Hao E; Yu J; Xie S; Zhang W; Wang G
[Ad] Endereço:Department of General Surgery, The First Hospital of Jilin University, Changchun, Jilin, China.
[Ti] Título:Up-regulation of miR-888-5p in hepatocellular carcinoma cell lines and its effect on malignant characteristics of cells.
[So] Source:J Biol Regul Homeost Agents;31(1):163-169, 2017 Jan-Mar.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:MicroRNA (miRNA) expression has been linked to the molecular pathogenesis of hepatocellular carcinoma (HCC). The aberrant expression of miRNA is involved in the processes of tumorigenesis and cancer progression. According to the latest research, miR-888-5p is associated with strong cancer-promoting effect. For instance, miR-888-5p is up-regulated in prostate cancer and breast cancer. Nevertheless, the role of miR-888-5p in HCC has not been investigated to date. In this study, we found that miR-888-5p levels in four HCC cell lines (SMMC7721, HepG2, Huh-7 and Bel7402) were significantly up-regulated compared with human hepatocyte cell line (HHL-5). After transiently transfected with miR-888-5p mimic, our results demonstrated that miR-888-5p plays a major role in promoting the proliferation and metastatic potential of HCC cells. Moreover, miR-888-5p also increased the expression of MMP-2 and MMP-9 proteins which account for cell migration and invasion, and decreased the expression of p53 protein which further promoted malignance of HCC. Therefore, miR-888-5p may be considered a potential biomarker for diagnostics and prognosis of HCC.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/genética
Regulação Neoplásica da Expressão Gênica
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 9 da Matriz/genética
MicroRNAs/genética
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/genética
Biomarcadores Tumorais/metabolismo
Linhagem Celular
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Transformação Celular Neoplásica/metabolismo
Transformação Celular Neoplásica/patologia
Células Hep G2
Hepatócitos/citologia
Hepatócitos/metabolismo
Seres Humanos
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
MicroRNAs/antagonistas & inibidores
MicroRNAs/metabolismo
Oligorribonucleotídeos Antissenso/genética
Oligorribonucleotídeos Antissenso/metabolismo
Transdução de Sinais
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (MIRN888 microRNA, human); 0 (MicroRNAs); 0 (Oligoribonucleotides, Antisense); 0 (Tumor Suppressor Protein p53); EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE


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[PMID]:28173844
[Au] Autor:Zhang W; Dong R; Diao S; Du J; Fan Z; Wang F
[Ad] Endereço:Department of Oral Basic Science, School of Stomatology, Dalian Medical University, Liaoning, 116044, China.
[Ti] Título:Differential long noncoding RNA/mRNA expression profiling and functional network analysis during osteogenic differentiation of human bone marrow mesenchymal stem cells.
[So] Source:Stem Cell Res Ther;8(1):30, 2017 Feb 07.
[Is] ISSN:1757-6512
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mesenchymal stem cells (MSCs) are the most promising cell types for bone regeneration and repair due to their osteogenic potential. MSC differentiation is precisely regulated and orchestrated by the mechanical and molecular signals from the extracellular environment, involving complex pathways regulated at both the transcriptional and post-transcriptional levels. However, the potential role of long noncoding RNA (lncRNA) in the osteogenic differentiation of human MSCs remains largely unclear. METHODS: Here, we undertook the survey of differential coding and noncoding transcript expression profiling and functional network analysis during osteogenic differentiation of human bone marrow mesenchymal stem cells (BMSCs) using human whole transcriptome microarray. The key pathways, mRNAs, and lncRNAs controlling osteogenic differentiation of BMSCs were identified by further bioinformatic analysis. The role of lncRNA in the osteogenic differentiation of MSCs was verified by lncRNA overexpression or knockdown methods. RESULTS: A total of 1269 coding transcripts with 648 genes significantly upregulated and 621 genes downregulated, and 1408 lncRNAs with 785 lncRNAs significantly upregulated and 623 lncRNAs downregulated were detected along with osteogenic differentiation. Bioinformatic analysis identified that several pathways may be associated with osteogenic differentiation potentials of BMSCs, such as the MAPK signaling pathway, the Jak-STAT signaling pathway, the Toll-like receptor signaling pathway, and the TGF-beta signaling pathway, etc. Bioinformatic analysis also revealed 13 core regulatory genes including seven mRNAs (GPX3, TLR2, BDKRB1, FBXO5, BRCA1, MAP3K8, and SCARB1), and six lncRNAs (XR_111050, NR_024031, FR374455, FR401275, FR406817, and FR148647). Based on the analysis, we identified one lncRNA, XR_111050, that could enhance the osteogenic differentiation potentials of MSCs. CONCLUSIONS: The potential regulatory mechanisms were identified using bioinformatic analyses. We further predicted the interactions of differentially expressed coding and noncoding genes, and identified core regulatory factors by co-expression networks during osteogenic differentiation of BMSCs. Our results could lead to a better understanding of the molecular mechanisms of genes and lncRNAs, and their cooperation underlying MSC osteogenic differentiation and bone formation. We identified that one lncRNA, XR_111050, could be a potential target for bone tissue engineering.
[Mh] Termos MeSH primário: Células Mesenquimais Estromais/metabolismo
Osteoblastos/metabolismo
Osteogênese/genética
RNA Longo não Codificante/genética
RNA Mensageiro/genética
Transcriptoma
[Mh] Termos MeSH secundário: Células da Medula Óssea/citologia
Células da Medula Óssea/metabolismo
Osso e Ossos/citologia
Osso e Ossos/metabolismo
Diferenciação Celular
Biologia Computacional
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Seres Humanos
Janus Quinases/genética
Janus Quinases/metabolismo
Células Mesenquimais Estromais/citologia
Análise de Sequência com Séries de Oligonucleotídeos
Oligorribonucleotídeos Antissenso/genética
Oligorribonucleotídeos Antissenso/metabolismo
Osteoblastos/citologia
RNA Longo não Codificante/antagonistas & inibidores
RNA Longo não Codificante/metabolismo
RNA Mensageiro/antagonistas & inibidores
RNA Mensageiro/metabolismo
Fatores de Transcrição STAT/genética
Fatores de Transcrição STAT/metabolismo
Transdução de Sinais
Receptores Toll-Like/genética
Receptores Toll-Like/metabolismo
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oligoribonucleotides, Antisense); 0 (RNA, Long Noncoding); 0 (RNA, Messenger); 0 (STAT Transcription Factors); 0 (Toll-Like Receptors); 0 (Transforming Growth Factor beta); EC 2.7.10.2 (Janus Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.1186/s13287-017-0485-6


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[PMID]:27484097
[Au] Autor:Suzuki K; Yokoyama J; Kawauchi Y; Honda Y; Sato H; Aoyagi Y; Terai S; Okazaki K; Suzuki Y; Sameshima Y; Fukushima T; Sugahara K; Atreya R; Neurath MF; Watanabe K; Yoneyama H; Asakura H
[Ad] Endereço:Department of Gastroenterology, Niigata University Medical and Dental Hospital, Niigata, Niigata, Japan kjsuzuki@med.niigata-u.ac.jp.
[Ti] Título:Phase 1 Clinical Study of siRNA Targeting Carbohydrate Sulphotransferase 15 in Crohn's Disease Patients with Active Mucosal Lesions.
[So] Source:J Crohns Colitis;11(2):221-228, 2017 Feb.
[Is] ISSN:1876-4479
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Carbohydrate sulphotransferase 15 [CHST15] is a specific enzyme biosynthesizing chondroitin sulphate E that binds various pathogenic mediators and is known to create local fibrotic lesions. We evaluated the safety of STNM01, a synthetic double-stranded RNA oligonucleotide directed against CHST15, in Crohn's disease [CD] patients whose mucosal lesions were refractory to conventional therapy. METHODS: This was a randomized, double-blind, placebo-controlled, concentration-escalation study of STNM01 by a single-dose endoscopic submucosal injection in 18 CD patients. Cohorts of increasing concentration of STNM01 were enrolled sequentially as 2.5nM [n = 3], 25nM [n = 3], and 250nM [n = 3] were applied. A cohort of placebo [n = 3] was included in each concentration. Safety was monitored for 30 days. Pharmacokinetics was monitored for 24h. The changes from baseline in the segmental Simple Endoscopic Score for CD [SES-CD] as well as the histological fibrosis score were evaluated. RESULTS: STNM01 was well tolerated and showed no drug-related adverse effects in any cohort of treated patients. There were no detectable plasma concentrations of STNM01 at all measured time points in all treatment groups. Seven of nine subjects who received STNM01 showed reduction in segmental SES-CD at Day 30, when compared with those who received placebo. Histological analyses of biopsy specimens revealed that STNM01 reduced the extent of fibrosis. CONCLUSION: Local application of STNM01 is safe and well tolerated in CD patients with active mucosal lesions.
[Mh] Termos MeSH primário: Sulfatos de Condroitina
Doença de Crohn
Mucosa Intestinal
Glicoproteínas de Membrana
RNA Interferente Pequeno/farmacologia
Sulfotransferases
[Mh] Termos MeSH secundário: Biópsia/métodos
Sulfatos de Condroitina/biossíntese
Sulfatos de Condroitina/metabolismo
Doença de Crohn/diagnóstico
Doença de Crohn/tratamento farmacológico
Doença de Crohn/patologia
Relação Dose-Resposta a Droga
Monitoramento de Medicamentos/métodos
Ressecção Endoscópica de Mucosa/métodos
Feminino
Fibrose
Fármacos Gastrointestinais/farmacologia
Seres Humanos
Injeções Intralesionais
Mucosa Intestinal/efeitos dos fármacos
Mucosa Intestinal/metabolismo
Mucosa Intestinal/patologia
Masculino
Glicoproteínas de Membrana/antagonistas & inibidores
Glicoproteínas de Membrana/metabolismo
Oligorribonucleotídeos Antissenso/farmacologia
Gravidade do Paciente
Sulfotransferases/antagonistas & inibidores
Sulfotransferases/metabolismo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (CHST15 protein, human); 0 (Gastrointestinal Agents); 0 (Membrane Glycoproteins); 0 (Oligoribonucleotides, Antisense); 0 (RNA, Small Interfering); 9007-28-7 (Chondroitin Sulfates); EC 2.8.2.- (Sulfotransferases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160804
[St] Status:MEDLINE
[do] DOI:10.1093/ecco-jcc/jjw143


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[PMID]:26724749
[Au] Autor:Crater AK; Roscoe S; Roberts M; Ananvoranich S
[Ad] Endereço:Department of Chemistry and Biochemistry, University of Windsor, Windsor, Ontario N9B3P4, Canada.
[Ti] Título:Antisense technologies in the studying of Toxoplasma gondii.
[So] Source:J Microbiol Methods;138:93-99, 2017 Jul.
[Is] ISSN:1872-8359
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This review covers a brief history of antisense RNAs and its applications, and summarizes the current stage of antisense technologies used in Toxoplasma gondii, a fascinating model organism with a unique characteristic blend of genetic regulatory systems normally found in plants or animals. Based on the current knowledge of regulatory RNAs and non-coding RNA (ncRNA), the antisense technologies are reviewed according to the classification of ncRNAs, which are roughly categorized into small, ranging from ~20-200 nucleotides in length, and long >200 nucleotides. Techniques utilizing small regulatory RNAs such as siRNA, miRNA, antagomirs, ribozymes and morpholino oligomers are discussed along with long non-coding RNA (lncRNA) including antisense and double stranded. These antisense technologies can be used in forward and reverse genetics studies. The future of technologies is limitless, particularly by combining these technologies with conventional methods, and should allow for ever greater understanding of gene regulation of the organism and related pathogenic microorganisms.
[Mh] Termos MeSH primário: MicroRNAs/genética
Oligorribonucleotídeos Antissenso/genética
RNA Interferente Pequeno/genética
Toxoplasma/genética
[Mh] Termos MeSH secundário: Antagomirs/genética
Morfolinos/genética
RNA Catalítico/genética
Toxoplasmose/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antagomirs); 0 (MicroRNAs); 0 (Morpholinos); 0 (Oligoribonucleotides, Antisense); 0 (RNA, Catalytic); 0 (RNA, Small Interfering)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160103
[St] Status:MEDLINE


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[PMID]:27906093
[Au] Autor:Yu L; Lu Y; Han X; Zhao W; Li J; Mao J; Wang B; Shen J; Fan S; Wang L; Wang M; Li L; Tang J; Song B
[Ad] Endereço:Department of Pathology, Dalian Medical University, Dalian, 116044, People's Republic of China.
[Ti] Título:microRNA -140-5p inhibits colorectal cancer invasion and metastasis by targeting ADAMTS5 and IGFBP5.
[So] Source:Stem Cell Res Ther;7(1):180, 2016 Dec 01.
[Is] ISSN:1757-6512
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Colorectal cancer (CRC) is one of the most common malignancies in the world. microRNA-140-5p (miR-140) has been shown to be involved in cartilage development and osteoarthritis (OA) pathogenesis. Some contradictions still exist concerning the role of miR-140 in tumor progression and metastasis, and the underlying mechanism is uncertain. METHODS: Immunohistochemistry was performed to determine the expressions of ADAMTS5 and IGFBP5 in CRC tissues. Human CRC cell lines HCT116 and RKO were transfected with miR-140 mimic, inhibitor, or small interfering RNA (siRNA) against ADAMTS5 or IGFBP5, respectively, using oligofectamine or lipofectamine 2000. Scratch-wound assay and transwell migration and invasion assays were used to evaluate the effects of miR-140 on the capabilities of migration and invasion. The levels of miR-140 and ADAMTS5 and IGFBP5 mRNA were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Western blot was performed to examine the expression of ADAMTS5 and IGFBP5 proteins. RESULTS: miR-140 was significantly reduced, whereas ADAMTS5 and IGFBP5 were upregulated, in the human CRC tissues compared to the corresponding normal colorectal mucosa. miR-140 downregulation and ADAMTS5 or IGFBP5 overexpression were associated with the advanced TNM stage and distant metastasis of CRC. There was a reverse correlation between miR-140 levels and ADAMTS5 and IGFBP5 expression in CRC tissues. ADAMTS5 and IGFBP5 were downregulated by miR-140 at both the protein and mRNA levels in the CRC cell lines. The gain-of- and loss-of-function studies showed that miR-140 inhibited CRC cell migratory and invasive capacities at least partially via downregulating the expression of ADAMTS5 and IGFBP5. CONCLUSIONS: These findings suggest that miR-140 suppresses CRC progression and metastasis, possibly through downregulating ADAMTS5 and IGFBP5. miR-140 might be a potential therapeutic candidate for the treatment of CRC.
[Mh] Termos MeSH primário: Proteína ADAMTS5/genética
Neoplasias Colorretais/genética
Regulação Neoplásica da Expressão Gênica
Proteína 5 de Ligação a Fator de Crescimento Semelhante à Insulina/genética
MicroRNAs/genética
[Mh] Termos MeSH secundário: Proteína ADAMTS5/antagonistas & inibidores
Proteína ADAMTS5/metabolismo
Idoso
Linhagem Celular Tumoral
Movimento Celular
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Progressão da Doença
Feminino
Células HCT116
Seres Humanos
Proteína 5 de Ligação a Fator de Crescimento Semelhante à Insulina/antagonistas & inibidores
Proteína 5 de Ligação a Fator de Crescimento Semelhante à Insulina/metabolismo
Masculino
MicroRNAs/antagonistas & inibidores
MicroRNAs/metabolismo
Meia-Idade
Invasividade Neoplásica
Metástase Neoplásica
Estadiamento de Neoplasias
Oligorribonucleotídeos Antissenso/genética
Oligorribonucleotídeos Antissenso/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin-Like Growth Factor Binding Protein 5); 0 (MicroRNAs); 0 (Mirn140 microRNA, human); 0 (Oligoribonucleotides, Antisense); 0 (RNA, Small Interfering); EC 3.4.24.- (ADAMTS5 Protein); EC 3.4.24.- (ADAMTS5 protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161202
[St] Status:MEDLINE


  8 / 393 MEDLINE  
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[PMID]:27886062
[Au] Autor:Wen X; Tang X; Li Y; Ren X; He Q; Yang X; Zhang J; Wang Y; Ma J; Liu N
[Ad] Endereço:Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, China. wenxin1@sysucc.org.cn.
[Ti] Título:Microarray Expression Profiling of Long Non-Coding RNAs Involved in Nasopharyngeal Carcinoma Metastasis.
[So] Source:Int J Mol Sci;17(11), 2016 Nov 23.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Increasing evidence has demonstrated a significant role for long non-coding RNAs (lncRNAs) in tumorigenesis. However, their functions in nasopharyngeal carcinoma (NPC) metastasis remain largely unknown. In this study, a model comparing high and low metastatic NPC cell lines (5-8F vs. 6-10B and S18 vs. S26) was constructed to determine the expression profile of lncRNAs using the microarray analysis, and we found 167 lncRNAs and 209 mRNAs were differentially expressed. Bioinformatic analysis indicated that the dysregulated mRNAs participated in important biological regulatory functions in NPC. Validation of 26 significantly dysregulated lncRNAs by qRT-PCR showed the expression patterns of 22 lncRNAs were in accordance with the microarray data. Furthermore, the expression level of ENST00000470135, which was the most upregulated lncRNA in high metastatic cell lines, was significantly higher in NPC cell lines and tissues with lymph node metastasis (LNM) and knocking down ENST00000470135 suppressed the migration, invasion and proliferation of NPC cells in vitro. In conclusion, our study revealed expression patterns of lncRNAs in NPC metastasis. The dysregulated lncRNAs may act as novel biomarkers and therapeutic targets for NPC.
[Mh] Termos MeSH primário: Carcinogênese/genética
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Neoplasias Nasofaríngeas/genética
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Carcinogênese/metabolismo
Carcinogênese/patologia
Carcinoma
Estudos de Casos e Controles
Linhagem Celular Tumoral
Movimento Celular
Biologia Computacional
Seres Humanos
Metástase Linfática
Análise em Microsséries
Neoplasias Nasofaríngeas/metabolismo
Neoplasias Nasofaríngeas/patologia
Análise de Sequência com Séries de Oligonucleotídeos
Oligorribonucleotídeos Antissenso/genética
Oligorribonucleotídeos Antissenso/metabolismo
RNA Longo não Codificante/antagonistas & inibidores
RNA Longo não Codificante/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oligoribonucleotides, Antisense); 0 (RNA, Long Noncoding); 0 (RNA, Messenger)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE


  9 / 393 MEDLINE  
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[PMID]:27706599
[Au] Autor:Zhang XH; Geng GL; Su B; Liang CP; Wang F; Bao JC
[Ad] Endereço:Department of Physical Therapy, Wuxi Tongren International Rehabilitation Hospital, Wuxi, Jiangsu, China.
[Ti] Título:MicroRNA-338-3p inhibits glucocorticoid-induced osteoclast formation through RANKL targeting.
[So] Source:Genet Mol Res;15(3), 2016 Aug 26.
[Is] ISSN:1676-5680
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:The differentiation deficiencies of osteoclast precursors (pre-OCs) may contribute to osteoporosis. Research on osteoporosis has recently focused on microRNAs (miRNAs) that play crucial roles in pre-OC differentiation. In the current study, we aimed to analyze the expression and function of the glucocorticoid (GC)-associated miRNA-338-3p (miR-338-3p) in osteoclast formation. We found that dexamethasone induced osteoclast differentiation and inhibited miR-338-3p expression. Overexpression of an miR-338-3p mimic in osteoclast precursor cells attenuated GC-induced osteoclast formation and bone resorption, whereas inhibition of miR-338-3p reversed these effects. The expression of the nuclear factor κB ligand RANKL, a potential target gene of miR-338-3p, was inversely correlated with miR-338-3p expression in pre-OCs. Furthermore, we demonstrated that RANKL was directly regulated by miR-338-3p and re-introduction of RANKL reversed the inhibitory effects of miR-338-3p on osteoclast formation and bone resorption. Taken together, these findings demonstrate that miR-338-3p may play a significant role in GC-induced osteoclast differentiation and function by targeting RANKL in osteoclasts.
[Mh] Termos MeSH primário: Reabsorção Óssea/genética
Dexametasona/farmacologia
Glucocorticoides/farmacologia
MicroRNAs/genética
Osteoclastos/efeitos dos fármacos
Ligante RANK/genética
[Mh] Termos MeSH secundário: Animais
Células da Medula Óssea/efeitos dos fármacos
Células da Medula Óssea/metabolismo
Células da Medula Óssea/patologia
Reabsorção Óssea/metabolismo
Reabsorção Óssea/patologia
Bovinos
Diferenciação Celular/efeitos dos fármacos
Técnicas de Cocultura
Feminino
Fêmur/efeitos dos fármacos
Fêmur/metabolismo
Fêmur/patologia
Regulação da Expressão Gênica
Camundongos
Camundongos Endogâmicos C57BL
MicroRNAs/antagonistas & inibidores
MicroRNAs/metabolismo
Modelos Biológicos
Oligorribonucleotídeos Antissenso/genética
Oligorribonucleotídeos Antissenso/metabolismo
Osteoblastos/citologia
Osteoblastos/efeitos dos fármacos
Osteoblastos/metabolismo
Osteoclastos/metabolismo
Osteoclastos/patologia
Cultura Primária de Células
Ligante RANK/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucocorticoids); 0 (MicroRNAs); 0 (Mirn338 microRNA, mouse); 0 (Oligoribonucleotides, Antisense); 0 (RANK Ligand); 0 (Tnfsf11 protein, mouse); 7S5I7G3JQL (Dexamethasone)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161006
[St] Status:MEDLINE
[do] DOI:10.4238/gmr.15037674


  10 / 393 MEDLINE  
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[PMID]:27681436
[Au] Autor:Diermeier SD; Chang KC; Freier SM; Song J; El Demerdash O; Krasnitz A; Rigo F; Bennett CF; Spector DL
[Ad] Endereço:Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
[Ti] Título:Mammary Tumor-Associated RNAs Impact Tumor Cell Proliferation, Invasion, and Migration.
[So] Source:Cell Rep;17(1):261-274, 2016 Sep 27.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Long non-coding RNAs (lncRNAs) represent the largest and most diverse class of non-coding RNAs, comprising almost 16,000 currently annotated transcripts in human and 10,000 in mouse. Here, we investigated the role of lncRNAs in mammary tumors by performing RNA-seq on tumor sections and organoids derived from MMTV-PyMT and MMTV-Neu-NDL mice. We identified several hundred lncRNAs that were overexpressed compared to normal mammary epithelium. Among these potentially oncogenic lncRNAs we prioritized a subset as Mammary Tumor Associated RNAs (MaTARs) and determined their human counterparts, hMaTARs. To functionally validate the role of MaTARs, we performed antisense knockdown and observed reduced cell proliferation, invasion, and/or organoid branching in a cancer-specific context. Assessing the expression of hMaTARs in human breast tumors revealed that 19 hMaTARs are significantly upregulated and many of these correlate with breast cancer subtype and/or hormone receptor status, indicating potential clinical relevance.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Neoplasias Mamárias Animais/terapia
Oligorribonucleotídeos Antissenso/genética
RNA Longo não Codificante/genética
RNA Neoplásico/genética
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Sobrevivência Celular
Feminino
Seres Humanos
Neoplasias Mamárias Animais/genética
Neoplasias Mamárias Animais/metabolismo
Neoplasias Mamárias Animais/patologia
Camundongos
Camundongos Transgênicos
Oligorribonucleotídeos Antissenso/metabolismo
Oligorribonucleotídeos Antissenso/uso terapêutico
RNA Longo não Codificante/antagonistas & inibidores
RNA Longo não Codificante/metabolismo
RNA Neoplásico/antagonistas & inibidores
RNA Neoplásico/metabolismo
Esferoides Celulares/metabolismo
Esferoides Celulares/patologia
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oligoribonucleotides, Antisense); 0 (RNA, Long Noncoding); 0 (RNA, Neoplasm)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160930
[St] Status:MEDLINE



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