Base de dados : MEDLINE
Pesquisa : D12.776.395.550.200.250.150.050 [Categoria DeCS]
Referências encontradas : 266 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 27 ir para página                         

  1 / 266 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29176323
[Au] Autor:He W; Huang L; Li M; Yang Y; Chen Z; Shen X
[Ti] Título:MiR-148b, MiR-152/ALCAM Axis Regulates the Proliferation and Invasion of Pituitary Adenomas Cells.
[So] Source:Cell Physiol Biochem;44(2):792-803, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Aberrant expression of miRNA has been found in many tumor tissues to regulate the tumorigenesis by binding to the 3`- untranslated region (3`-UTR) of the target genes. The aim of this study is to investigate the role of miR-148b, miR-152/ALCAM axis in human pituitary adenomas (PAs). METHODS: First, we detected the expression level of miR-148b-3p and miR-152 in human PAs samples by using qRT-PCR. Then we studied the role of miR-148b-3p, miR-152 on human PAs cell proliferation, invasion and apoptosis by using MTS assay, Transwell invasion assay and Annexin V/PI Staining Test. To study the relationship between miR-148b-3p, miR-152 and activated leukocyte antigen molecule (ALCAM), we overexpressed miR-148-3p or miR-152 by transfecting specific mimics. Lucifearase reporter assay was then performed to confirm the target. Next, we studied the biological functions of ALCAM in human PAs cells. Finally, the role of miR-148b-3p, miR-152/ALCAM axis in PAs cells was studied. RESULTS: The expression level of miR-148-3p and miR-152 in invasive PAs samples was lower than those in noninvasive samples. Overexpression of miR-148b-3p, miR-152 could repress proliferation and invasion, and promote apoptosis. Moreover, miR-148b-3p and miR-152 could repress activated leukocyte antigen molecule (ALCAM) expression. Knockdown of ALCAM could repress proliferation and invasion and promote apoptosis. By contrary, overexpression of ALCAM promoted proliferation and invasion. Further, the rescue experiments indicated that overexpression of ALCAM significantly restored the proliferation, apoptosis, and invasion influenced by miR-148b-3p and miR-152. CONCLUSIONS: Our study suggests that miR-148b-3p, miR-152 may serve as suppressors in PAs through downregulating ALCAM expression. miR-148b, miR-152/ ALCAM axis may be a new therapeutic target in the future.
[Mh] Termos MeSH primário: Molécula de Adesão de Leucócito Ativado/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Molécula de Adesão de Leucócito Ativado/química
Molécula de Adesão de Leucócito Ativado/genética
Animais
Antagomirs/metabolismo
Sequência de Bases
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Ensaio de Imunoadsorção Enzimática
Hormônio do Crescimento/análise
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Neoplasias Hipofisárias/metabolismo
Neoplasias Hipofisárias/patologia
Prolactina/análise
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Ratos
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Activated-Leukocyte Cell Adhesion Molecule); 0 (Antagomirs); 0 (MicroRNAs); 0 (RNA, Small Interfering); 9002-62-4 (Prolactin); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485342


  2 / 266 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28465351
[Au] Autor:Morimoto A; Kannari M; Tsuchida Y; Sasaki S; Saito C; Matsuta T; Maeda T; Akiyama M; Nakamura T; Sakaguchi M; Nameki N; Gonzalez FJ; Inoue Y
[Ad] Endereço:From the Laboratory of Molecular Life Science, Division of Molecular Science, Faculty of Science and Technology, Gunma University, Kiryu, Gunma 376-8515, Japan.
[Ti] Título:An HNF4α-microRNA-194/192 signaling axis maintains hepatic cell function.
[So] Source:J Biol Chem;292(25):10574-10585, 2017 06 23.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatocyte nuclear factor 4α (HNF4α) controls the expression of liver-specific protein-coding genes. However, some microRNAs are also modulated by HNF4α, and it is not known whether they are direct targets of HNF4α and whether they influence hepatic function. In this study, we found that HNF4α regulates microRNAs, indicated by marked down-regulation of miR-194 and miR-192 (miR-194/192) in liver-specific -null ( ) mice. Transactivation of the shared miR-194/192 promoter was dependent on HNF4α expression, indicating that miR-194/192 is a target gene of HNF4α. Screening of potential mRNAs targeted by miR-194/192 revealed that expression of genes involved in glucose metabolism (glycogenin 1 ( )), cell adhesion and migration (activated leukocyte cell adhesion molecule ( )), tumorigenesis and tumor progression ( and epiregulin ( )), protein SUMOylation ( ), epigenetic regulation ( and Cullin 4B ( )), and the epithelial-mesenchymal transition (moesin ( )) was up-regulated in mice. Moreover, we also found that miR-194/192 binds the 3'-UTR of these mRNAs. siRNA knockdown of HNF4α suppressed miR-194/192 expression in human hepatocellular carcinoma (HCC) cells and resulted in up-regulation of their mRNA targets. Inhibition and overexpression experiments with miR-194/192 revealed that , , , , and are miR-194 targets, whereas , , and are miR-192 targets. These findings reveal a novel HNF4α network controlled by miR-194/192 that may play a critical role in maintaining the hepatocyte-differentiated state by inhibiting expression of genes involved in dedifferentiation and tumorigenesis. These insights may contribute to the development of diagnostic markers for early HCC detection, and targeting of the miR-194/192 pathway could be useful for managing HCC.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/fisiologia
Fator 4 Nuclear de Hepatócito/metabolismo
Hepatócitos/metabolismo
MicroRNAs/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/fisiologia
Molécula de Adesão de Leucócito Ativado/biossíntese
Molécula de Adesão de Leucócito Ativado/genética
Animais
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Epirregulina/biossíntese
Epirregulina/genética
Glucosiltransferases/biossíntese
Glucosiltransferases/genética
Glicoproteínas/biossíntese
Glicoproteínas/genética
Fator 4 Nuclear de Hepatócito/genética
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/metabolismo
Camundongos
Camundongos Mutantes
MicroRNAs/genética
Proteínas dos Microfilamentos/biossíntese
Proteínas dos Microfilamentos/genética
Proteínas Modificadoras Pequenas Relacionadas à Ubiquitina/biossíntese
Proteínas Modificadoras Pequenas Relacionadas à Ubiquitina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Activated-Leukocyte Cell Adhesion Molecule); 0 (Epiregulin); 0 (Ereg protein, mouse); 0 (Glycoproteins); 0 (Hepatocyte Nuclear Factor 4); 0 (Hnf4a protein, mouse); 0 (MIRN194 microRNA, mouse); 0 (MicroRNAs); 0 (Microfilament Proteins); 0 (Mirn192 microRNA, mouse); 0 (SUMO2 protein, mouse); 0 (Small Ubiquitin-Related Modifier Proteins); 0 (glycogenin); 144131-77-1 (moesin); EC 2.4.1.- (Glucosyltransferases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.785592


  3 / 266 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28817794
[Au] Autor:Thoumine O; Marchot P
[Ad] Endereço:Interdisciplinary Institute for Neuroscience, UMR 5297, Centre National de la Recherche Scientifique, University of Bordeaux, 33000 Bordeaux, France. Electronic address: olivier.thoumine@u-bordeaux.fr.
[Ti] Título:A Triad of Crystals Sheds Light on MDGA Interference with Neuroligation.
[So] Source:Neuron;95(4):729-732, 2017 Aug 16.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neurexins and neuroligins form trans-synaptic complexes that promote synapse development. In this issue of Neuron, Aricescu and colleagues (Elegheert et al., 2017) complement and strengthen two recent reports by the Kim and Rudenko teams (Kim et al., 2017; Gangwar et al., 2017) to dissect the molecular determinants by which MDGAs challenge the neurexin-neuroligin partnership.
[Mh] Termos MeSH primário: Compostos de Dansil/metabolismo
Galactosamina/análogos & derivados
Sinapses/fisiologia
[Mh] Termos MeSH secundário: Molécula de Adesão de Leucócito Ativado/metabolismo
Animais
Moléculas de Adesão Celular Neuronais/metabolismo
Galactosamina/metabolismo
Complexos Multiproteicos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activated-Leukocyte Cell Adhesion Molecule); 0 (Cell Adhesion Molecules, Neuronal); 0 (Dansyl Compounds); 0 (Multiprotein Complexes); 146440-32-6 (methyl-N-dansylgalactosaminide); 7535-00-4 (Galactosamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE


  4 / 266 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28427856
[Au] Autor:Seigfried FA; Cizelsky W; Pfister AS; Dietmann P; Walther P; Kühl M; Kühl SJ
[Ad] Endereço:Institute of Biochemistry and Molecular Biology, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany; International Graduate School in Molecular Medicine Ulm, 89081 Ulm, Germany; Tissue Homeostasis Joint-PhD-Programme in Cooperation with the University of Oulu, Finland.
[Ti] Título:Frizzled 3 acts upstream of Alcam during embryonic eye development.
[So] Source:Dev Biol;426(1):69-83, 2017 06 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Formation of a functional eye during vertebrate embryogenesis requires different processes such as cell differentiation, cell migration, cell-cell interactions as well as intracellular signalling processes. It was previously shown that the non-canonical Wnt receptor Frizzled 3 (Fzd3) is required for proper eye formation, however, the underlying mechanism is poorly understood. Here we demonstrate that loss of Fzd3 induces severe malformations of the developing eye and that this defect is phenocopied by loss of the activated leukocyte cell adhesion molecule (Alcam). Promoter analysis revealed the presence of a Fzd3 responsive element within the alcam promoter, which is responsible for alcam expression during anterior neural development. In-depth analysis identified the jun N-terminal protein kinase 1 (JNK1) and the transcription factor paired box 2 (Pax2) to be important for the activation of alcam expression. Altogether our study reveals that alcam is activated through non-canonical Wnt signalling during embryonic eye development in Xenopus laevis and shows that this pathway plays a similar role in different tissues.
[Mh] Termos MeSH primário: Molécula de Adesão de Leucócito Ativado/genética
Olho/embriologia
Receptores Frizzled/genética
Proteínas de Xenopus/genética
Xenopus laevis/embriologia
[Mh] Termos MeSH secundário: Molécula de Adesão de Leucócito Ativado/metabolismo
Animais
Adesão Celular/fisiologia
Comunicação Celular/fisiologia
Diferenciação Celular/fisiologia
Movimento Celular/fisiologia
Olho/ultraestrutura
Receptores Frizzled/metabolismo
Técnicas de Inativação de Genes
Microscopia Eletrônica de Transmissão
Proteína Quinase 8 Ativada por Mitógeno/metabolismo
Morfolinos/genética
Neurogênese/genética
Neurogênese/fisiologia
Fator de Transcrição PAX2/metabolismo
Regiões Promotoras Genéticas/genética
Via de Sinalização Wnt
Proteínas de Xenopus/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Activated-Leukocyte Cell Adhesion Molecule); 0 (Frizzled Receptors); 0 (Morpholinos); 0 (PAX2 Transcription Factor); 0 (Xenopus Proteins); 0 (fz3 protein, Xenopus); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 8)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE


  5 / 266 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27992415
[Au] Autor:Park RJ; Wang T; Koundakjian D; Hultquist JF; Lamothe-Molina P; Monel B; Schumann K; Yu H; Krupzcak KM; Garcia-Beltran W; Piechocka-Trocha A; Krogan NJ; Marson A; Sabatini DM; Lander ES; Hacohen N; Walker BD
[Ad] Endereço:Ragon Institute of Massachusetts General Hospital (MGH), Massachusetts Institute of Technology (MIT), and Harvard University, Cambridge, Massachusetts, USA.
[Ti] Título:A genome-wide CRISPR screen identifies a restricted set of HIV host dependency factors.
[So] Source:Nat Genet;49(2):193-203, 2017 Feb.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Host proteins are essential for HIV entry and replication and can be important nonviral therapeutic targets. Large-scale RNA interference (RNAi)-based screens have identified nearly a thousand candidate host factors, but there is little agreement among studies and few factors have been validated. Here we demonstrate that a genome-wide CRISPR-based screen identifies host factors in a physiologically relevant cell system. We identify five factors, including the HIV co-receptors CD4 and CCR5, that are required for HIV infection yet are dispensable for cellular proliferation and viability. Tyrosylprotein sulfotransferase 2 (TPST2) and solute carrier family 35 member B2 (SLC35B2) function in a common pathway to sulfate CCR5 on extracellular tyrosine residues, facilitating CCR5 recognition by the HIV envelope. Activated leukocyte cell adhesion molecule (ALCAM) mediates cell aggregation, which is required for cell-to-cell HIV transmission. We validated these pathways in primary human CD4 T cells through Cas9-mediated knockout and antibody blockade. Our findings indicate that HIV infection and replication rely on a limited set of host-dispensable genes and suggest that these pathways can be studied for therapeutic intervention.
[Mh] Termos MeSH primário: Repetições Palindrômicas Curtas Agrupadas e Regularmente Espaçadas/genética
Infecções por HIV/genética
Interações Hospedeiro-Patógeno/genética
[Mh] Termos MeSH secundário: Molécula de Adesão de Leucócito Ativado/genética
Linhagem Celular
Genoma/genética
HIV-1/patogenicidade
Seres Humanos
Proteínas de Membrana/genética
Interferência de RNA/fisiologia
Receptores CCR5/genética
Sulfotransferases/genética
Replicação Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activated-Leukocyte Cell Adhesion Molecule); 0 (CCR5 protein, human); 0 (Membrane Proteins); 0 (Receptors, CCR5); EC 2.8.2.- (Sulfotransferases); EC 2.8.2.20 (TPST2 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171014
[Lr] Data última revisão:
171014
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161220
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3741


  6 / 266 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27573419
[Au] Autor:Zhang WW; Zhan SH; Geng CX; Sun X; Erkan M; Kleeff J; Xie XJ
[Ad] Endereço:Department of Gastroenterology, Qingdao Municipal Hospital, Qingdao, Shandong 266071, P.R. China.
[Ti] Título:Activated leukocyte cell adhesion molecule regulates the interaction between pancreatic cancer cells and stellate cells.
[So] Source:Mol Med Rep;14(4):3627-33, 2016 Oct.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Activated leukocyte cell adhesion molecule (ALCAM/CD166) is a transmembrane glycoprotein that is involved in tumor progression and metastasis. In the present study, the expression and functional role of ALCAM in pancreatic cancer cells and pancreatic stellate cells (PSCs) was investigated. Tissue specimens were obtained from patients with pancreatic ductal adenocarcinoma (n=56) or chronic pancreatitis (CP; n=10), who underwent pancreatic resection, and from normal pancreatic tissue samples (n=10). Immunohistochemistry was used to analyze the localization and expression of ALCAM in pancreatic tissues. Subsequently, reverse transcription­quantitative polymerase chain reaction and immunoblotting were applied to assess the expression of ALCAM in pancreatic cancer Panc­1 and T3M4 cells, as well as in PSCs. An enzyme­linked immunosorbent assay was used to measure ALCAM levels in cell culture medium stimulated by hypoxia, tumor necrosis factor (TNF)­α and transforming growth factor­ß. Silencing of ALCAM was performed using ALCAM small interfering (si)RNA and immunocytochemistry was used to analyze the inhibition efficiency. An invasion assay and a cell interaction assay were performed to assess the invasive ability and co­cultured adhesive potential of Panc­1 and T3M4 cells, as well as PSCs. Histologically, ALCAM expression was generally weak or absent in pancreatic cancer cells, but was markedly upregulated in PSCs in pancreatic cancer tissues. ALCAM was highly expressed in PSCs from CP tissues and PSCs surrounding pancreatic intraepithelial neoplasias, as well as in pancreatic cancer cells. ALCAM mRNA was highly expressed in PSCs, with a low to moderate expression in T3M4 and Panc­1 cells. Similar to the mRNA expression, immunoblotting demonstrated that ALCAM protein levels were high in PSCs and T3M4 cells, but low in Panc­1 cells. The expression of TNF­α increased, while hypoxia decreased the secretion of ALCAM in pancreatic cancer Panc­1 and T3M4 cells, and also in PSCs. Silencing of ALCAM by siRNA revealed no significant alteration in the invasion of pancreatic cancer cells, however, it inhibited the invasive ability of PSCs, and decreased the interaction between Panc­1 cells and PSCs. In conclusion, ALCAM is upregulated in PSCs of pancreatic cancer tissues, suggesting a potential role of ALCAM in regulating pancreatic cancer cell­PSC interactions.
[Mh] Termos MeSH primário: Molécula de Adesão de Leucócito Ativado/análise
Carcinoma Ductal Pancreático/patologia
Pâncreas/patologia
Neoplasias Pancreáticas/patologia
Células Estreladas do Pâncreas/patologia
[Mh] Termos MeSH secundário: Molécula de Adesão de Leucócito Ativado/genética
Carcinoma Ductal Pancreático/genética
Carcinoma Ductal Pancreático/metabolismo
Comunicação Celular
Linhagem Celular
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Pâncreas/citologia
Pâncreas/metabolismo
Neoplasias Pancreáticas/genética
Células Estreladas do Pâncreas/citologia
Células Estreladas do Pâncreas/metabolismo
Pancreatite/genética
Pancreatite/patologia
RNA Mensageiro/genética
RNA Interferente Pequeno/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activated-Leukocyte Cell Adhesion Molecule); 0 (RNA, Messenger); 0 (RNA, Small Interfering)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170413
[Lr] Data última revisão:
170413
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160831
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2016.5681


  7 / 266 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27409608
[Au] Autor:Winkler S; Hempel M; Brückner S; Tautenhahn HM; Kaufmann R; Christ B
[Ad] Endereço:Applied Molecular Hepatology Laboratory, Department of Visceral, Transplantation, Thoracic and Vascular Surgery, University Hospital of Leipzig, Liebigstraße 21, 04103 Leipzig, Germany. sandra.pelz@medizin.uni-leipzig.de.
[Ti] Título:Identification of Pathways in Liver Repair Potentially Targeted by Secretory Proteins from Human Mesenchymal Stem Cells.
[So] Source:Int J Mol Sci;17(7), 2016 Jul 09.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The beneficial impact of mesenchymal stem cells (MSC) on both acute and chronic liver diseases has been confirmed, although the molecular mechanisms behind it remain elusive. We aim to identify factors secreted by undifferentiated and hepatocytic differentiated MSC in vitro in order to delineate liver repair pathways potentially targeted by MSC. METHODS: Secreted factors were determined by protein arrays and related pathways identified by biomathematical analyses. RESULTS: MSC from adipose tissue and bone marrow expressed a similar pattern of surface markers. After hepatocytic differentiation, CD54 (intercellular adhesion molecule 1, ICAM-1) increased and CD166 (activated leukocyte cell adhesion molecule, ALCAM) decreased. MSC secreted different factors before and after differentiation. These comprised cytokines involved in innate immunity and growth factors regulating liver regeneration. Pathway analysis revealed cytokine-cytokine receptor interactions, chemokine signalling pathways, the complement and coagulation cascades as well as the Januskinase-signal transducers and activators of transcription (JAK-STAT) and nucleotide-binding oligomerization domain-like receptor (NOD-like receptor) signalling pathways as relevant networks. Relationships to transforming growth factor ß (TGF-ß) and hypoxia-inducible factor 1-α (HIF1-α) signalling seemed also relevant. CONCLUSION: MSC secreted proteins, which differed depending on cell source and degree of differentiation. The factors might address inflammatory and growth factor pathways as well as chemo-attraction and innate immunity. Since these are prone to dysregulation in most liver diseases, MSC release hepatotropic factors, potentially supporting liver regeneration.
[Mh] Termos MeSH primário: Molécula de Adesão de Leucócito Ativado/metabolismo
Citocinas/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Fígado/metabolismo
Células Mesenquimais Estromais/metabolismo
[Mh] Termos MeSH secundário: Tecido Adiposo/citologia
Células da Medula Óssea/citologia
Diferenciação Celular
Células Cultivadas
Quimiocinas/metabolismo
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Fígado/citologia
Regeneração Hepática/fisiologia
Células Mesenquimais Estromais/citologia
Proteínas NLR/metabolismo
Fenótipo
Transdução de Sinais
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activated-Leukocyte Cell Adhesion Molecule); 0 (Chemokines); 0 (Cytokines); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (NLR Proteins); 0 (Transforming Growth Factor beta); 126547-89-5 (Intercellular Adhesion Molecule-1)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160714
[St] Status:MEDLINE


  8 / 266 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27381622
[Au] Autor:Zheng Y; Wang Q; Li T; Qian J; Lu Y; Li Y; Bi E; Reu F; Qin Y; Drazba J; Hsi E; Yang J; Cai Z; Yi Q
[Ad] Endereço:Affiliations of authors: Department of Hematology and State Key Laboratory of Biotherapy and Cancer Center, Sichuan University, West China Hospital, China (YZ); Department of Cancer Biology (YZ, QW, TL, JQ, YLu, YLi, EB, QY), Taussig Cancer Center (FR), Imaging Core Facility, Lerner Research Institu
[Ti] Título:Role of Myeloma-Derived MIF in Myeloma Cell Adhesion to Bone Marrow and Chemotherapy Response.
[So] Source:J Natl Cancer Inst;108(11), 2016 Nov.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Multiple myeloma (MM) remains an incurable cancer characterized by accumulation of malignant plasma cells in the bone marrow (BM). The mechanism underlying MM homing to BM is poorly elucidated. METHODS: The clinical significance of migration inhibitory factor (MIF) expression was examined by analyzing six independent gene expression profile databases of primary MM cells using the Student's t test and Kaplan-Meier test. Enzyme-linked immunosorbent assay was used to examine MIF expression. In vivo bioluminescent imaging was used to determine MM cell localization and treatment efficacy in human MM xenograft mouse models, with three to four mice per group. MM cell attachment to BM stromal cells (BMSCs) was monitored by cell adhesion assay. MIF regulation of the expression of adhesion molecules was determined by chromatin immunoprecipitation (ChIP) assay. Statistical tests were two-sided. RESULTS: High levels of MIF were detected in MM BM (MIF level in BM plasma: healthy = 10.72 ± 5.788 ng/mL, n = 5; MM = 1811 ± 248.7 ng/mL, n = 10; P < .001) and associated with poor survival of patients (Kaplan-Meier test for MM OS: 87 MIF(high) patients, 86 MIF(low) patients, P = .02). Knocking down MIF impaired MM cell adhesion to BMSCs in vitro and led to formation of extramedullary tumors in SCID mice. MIF acted through surface receptor CXCR4 and adaptor COPS5 to regulate the expression of adhesion molecules ALCAM, ITGAV, and ITGB5 on MM cells. More importantly, MIF-deficient MM cells were sensitive to chemotherapy in vitro when cocultured with BMSCs and in vivo. MIF inhibitor 4-IPP sensitized MM cells to chemotherapy. CONCLUSIONS: MIF is an important player and a novel therapeutic target in MM. Inhibiting MIF activity will sensitize MM cells to chemotherapy.
[Mh] Termos MeSH primário: Resistência a Medicamentos Antineoplásicos/genética
Oxirredutases Intramoleculares/genética
Oxirredutases Intramoleculares/metabolismo
Fatores Inibidores da Migração de Macrófagos/genética
Fatores Inibidores da Migração de Macrófagos/metabolismo
Mieloma Múltiplo/genética
Mieloma Múltiplo/metabolismo
Plasmócitos/metabolismo
[Mh] Termos MeSH secundário: Molécula de Adesão de Leucócito Ativado/genética
Animais
Antígenos de Diferenciação de Linfócitos B/genética
Antígenos de Diferenciação de Linfócitos B/metabolismo
Antineoplásicos Alquilantes/farmacologia
Apoptose/efeitos dos fármacos
Comunicação Autócrina
Medula Óssea/metabolismo
Bortezomib/farmacologia
Complexo do Signalossomo COP9
Adesão Celular/efeitos dos fármacos
Adesão Celular/genética
Linhagem Celular Tumoral
Quimiotaxia/genética
Técnicas de Cocultura
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Feminino
Expressão Gênica
Técnicas de Silenciamento de Genes
Xenoenxertos
Antígenos de Histocompatibilidade Classe II/genética
Antígenos de Histocompatibilidade Classe II/metabolismo
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Oxirredutases Intramoleculares/antagonistas & inibidores
Fatores Inibidores da Migração de Macrófagos/antagonistas & inibidores
Melfalan/farmacologia
Células Mesenquimais Estromais/metabolismo
Camundongos
Camundongos SCID
Mieloma Múltiplo/tratamento farmacológico
Mieloma Múltiplo/patologia
Transplante de Neoplasias
Peptídeo Hidrolases/metabolismo
Pirimidinas/farmacologia
RNA Mensageiro/metabolismo
Receptores CXCR4/genética
Receptores CXCR4/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-iodo-6-phenylpyrimidine); 0 (Activated-Leukocyte Cell Adhesion Molecule); 0 (Antigens, Differentiation, B-Lymphocyte); 0 (Antineoplastic Agents, Alkylating); 0 (Histocompatibility Antigens Class II); 0 (Intracellular Signaling Peptides and Proteins); 0 (Macrophage Migration-Inhibitory Factors); 0 (Pyrimidines); 0 (RNA, Messenger); 0 (Receptors, CXCR4); 0 (invariant chain); 69G8BD63PP (Bortezomib); EC 3.4.- (Peptide Hydrolases); EC 3.4.-.- (COPS5 protein, human); EC 3.4.19.12 (COP9 Signalosome Complex); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.2.1 (MIF protein, human); Q41OR9510P (Melphalan)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160707
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djw131


  9 / 266 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27208904
[Au] Autor:Kudo-Saito C; Fuwa T; Kawakami Y
[Ad] Endereço:Institute for Advanced Medical Research, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Electronic address: kudoc@a3.keio.jp.
[Ti] Título:Targeting ALCAM in the cryo-treated tumour microenvironment successfully induces systemic anti-tumour immunity.
[So] Source:Eur J Cancer;62:54-61, 2016 Jul.
[Is] ISSN:1879-0852
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cryoablative treatment has been widely used for treating cancer. However, the therapeutic efficacies are still controversial. The molecular mechanisms of the cryo-induced immune responses, particularly underlying the ineffectiveness, remain to be fully elucidated. In this study, we identified a new molecular mechanism involved in the cryo failure. We used cryo-ineffective metastatic tumour models that murine melanoma B16-F10 cells were subcutaneously and intravenously implanted into C57BL/6 mice. When the subcutaneous tumours were treated cryoablation on day 7 after tumour implantation, cells expressing activated leucocyte cell adhesion molecule (ALCAM/CD166) were significantly expanded not only locally in the treated tumours but also systemically in spleen and bone marrow of the mice. The cryo-induced ALCAM(+) cells including CD45(-) mesenchymal stem/stromal cells, CD11b(+)Gr1(+) myeloid-derived suppressor cells, and CD4(+)Foxp3(+) regulatory T cells significantly suppressed interferon γ production and cytotoxicity of tumour-specific CD8(+) T cells via ALCAM expressed in these cells. This suggests that systemic expansion of the ALCAM(+) cells negatively switches host-immune directivity to the tumour-supportive mode. Intratumoural injection with anti-ALCAM blocking monoclonal antibody (mAb) following the cryo treatment systemically induced tumour-specific CD8(+) T cells with higher cytotoxic activities, resulting in suppression of tumour growth and metastasis in the cryo-resistant tumour models. These suggest that expansion of ALCAM(+) cells is a determinant of limiting the cryo efficacy. Further combination with an immune checkpoint inhibitor anti-CTLA4 mAb optimized the anti-tumour efficacy of the dual-combination therapy. Targeting ALCAM may be a promising strategy for overcoming the cryo ineffectiveness leading to the better practical use of cryoablation in clinical treatment of cancer.
[Mh] Termos MeSH primário: Técnicas de Ablação/métodos
Molécula de Adesão de Leucócito Ativado/fisiologia
Criocirurgia/métodos
Melanoma Experimental/cirurgia
Neoplasias Cutâneas/cirurgia
Microambiente Tumoral/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/uso terapêutico
Antígenos CD
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Moléculas de Adesão Celular Neuronais
Linhagem Celular Tumoral
Proteínas Fetais
Citometria de Fluxo
Interferon gama/metabolismo
Melanoma Experimental/patologia
Camundongos
Camundongos Endogâmicos C57BL
Neoplasias Cutâneas/patologia
Linfócitos T Reguladores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ALCAM protein, human); 0 (Activated-Leukocyte Cell Adhesion Molecule); 0 (Antibodies, Monoclonal); 0 (Antigens, CD); 0 (Cell Adhesion Molecules, Neuronal); 0 (Fetal Proteins); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160523
[St] Status:MEDLINE


  10 / 266 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27062566
[Au] Autor:Ribeiro KB; da Silva Zanetti J; Ribeiro-Silva A; Rapatoni L; de Oliveira HF; da Cunha Tirapelli DP; Garcia SB; Feres O; da Rocha JJ; Peria FM
[Ad] Endereço:Internal Medicine Department, School of Medicine of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
[Ti] Título:KRAS mutation associated with CD44/CD166 immunoexpression as predictors of worse outcome in metastatic colon cancer.
[So] Source:Cancer Biomark;16(4):513-21, 2016 Mar 04.
[Is] ISSN:1875-8592
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Multiple stages of carcinogenesis in colon cancer encompass subpopulations of cancer stem cells (CSC), responsible for tumor cell transformation, growth and proliferation. CD44 and CD166 proteins are CSC markers associated with cell signaling, adhesion, migration, metastasis and lymphocytic response. The expression of CSC may be modulated by some factors, such as the KRAS gene mutation. OBJECTIVE: Correlate the expression of CD44 and CD166 markers in metastatic colon adenocarcinoma and KRAS mutation status (wild-type/mutated) with clinical pathological features and patients' outcome. MATERIAL AND METHODS: Fifty-eight samples of tumor tissue samples of metastatic colon adenocarcinoma were collected from patients treated with CapeOx at the HCFMRP-USP Clinical Oncology Service. Clinical and survival data were collected from medical records. KRAS status was determined by the polymerase chain reaction (PCR) technique, and analysis of immunohistochemical expression of CD44 and CD166 proteins was performed by tissue microarray. RESULTS: The expression of CD44 and CD166 were positive in 41% and 43% of patients, respectively, and mutated KRAS was detected in 48% of patients. A significant association was found between CD166 and CD44 expression (p= 0.016), mainly in the wild-type KRAS group (p= 0.042) and patients over 65 years (p= 0.001). CD44-positive patients had 3.7-fold and 5.3-fold greater risk of liver metastasis and lung metastasis, respectively (p< 0.01), compared with CD44-negative patients. CD166-negative patients had 2.7 greater risk of lymph node involvement (0.03), compared with CD166-positive patients. KRAS mutation increased the risk of liver metastasis by 8 times (p< 0.01), and the risk of lung metastasis by 5 times (p= 0.04) in CD44-positive patients. KRAS mutation increased the risk of lymph node involvement by 8 times in CD166-negative patients (p= 0.0007). CONCLUSION: An association between CD44 and CD166 expression was demonstrated in this study. Analysis of KRAS mutation combined with immunohistochemical expression of CD44 and CD166 identified subgroups of patients with colon adenocarcinoma at higher risk of lymph node involvement by the tumor and development of liver and lung metastasis.
[Mh] Termos MeSH primário: Molécula de Adesão de Leucócito Ativado/metabolismo
Neoplasias do Colo/genética
Neoplasias do Colo/metabolismo
Receptores de Hialuronatos/metabolismo
Mutação
Proteínas ras/genética
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais
Neoplasias do Colo/mortalidade
Neoplasias do Colo/patologia
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Gradação de Tumores
Metástase Neoplásica
Estadiamento de Neoplasias
Células-Tronco Neoplásicas/metabolismo
Avaliação de Resultados da Assistência ao Paciente
Prognóstico
Modelos de Riscos Proporcionais
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activated-Leukocyte Cell Adhesion Molecule); 0 (Biomarkers, Tumor); 0 (Hyaluronan Receptors); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160411
[St] Status:MEDLINE
[do] DOI:10.3233/CBM-160592



página 1 de 27 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde