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[PMID]: 28698144 [Au] Autor: Setiawan M; Tan XW; Goh TW; Hin-Fai Yam G; Mehta JS [Ad] Endereço: Tissue Engineering and Stem Cell Group, Singapore Eye Research Institute, Singapore. [Ti] Título: Inhibiting glycogen synthase kinase-3 and transforming growth factor-ß signaling to promote epithelial transition of human adipose mesenchymal stem cells. [So] Source: Biochem Biophys Res Commun;490(4):1381-1388, 2017 Sep 02. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: BACKGROUND: This study was aimed to investigate the epithelial differentiation of human adipose-derived mesenchymal stem cells (ADSCs) by inhibiting glycogen synthase kinase-3 (GSK3) and transforming growth factor ß (TGFß) signaling. METHODS AND RESULTS: STEMPRO human ADSCs at passage 2 were treated with CHIR99021 (GSK3 inhibitor), E-616452 (TGFß1 receptor kinase inhibitor), A-83-01 (TGFß type 1 receptor inhibitor), valproic acid (histone deacetylase inhibitor), tranylcypromine (monoamine oxidase inhibitor) and all-trans retinoic acid for 72 h. The mesenchymal-epithelial transition was shown by down-regulation of mesenchymal genes (Slug, Zinc Finger E-box Binding Homeobox 1 ZEB1, integrin α5 ITGA5 and vimentin VIM) and up-regulation of epithelial genes (E-cadherin, Epithelial Cell Adhesion Molecule EpCAM, Zonula Occludens-1 ZO-1, occludin, deltaN p63 δNp63, Transcription Factor 4 TCF4 and Twist Family bHLH Transcription Factor TWIST), compared to untreated ADSCs. Cell morphology and stress fiber pattern were examined and the treated cells became less migratory in scratch wound closure assay. The formation of cell junction complexes was observed under transmission electron microscopy. Global gene expression using GeneChip Human Genome U133 Array (Affymetrix) showed that the treatment up-regulated 540 genes (containing genes for cell cycle, cytoskeleton reorganization, chemotaxis, epithelium development and regulation of cell migration) and down-regulated 483 genes. CONCLUSION: Human ADSCs were transited to epithelial lineage by inhibiting GSK3 and TGFß signaling. It can be an adult stem cell source for epithelial cell-based therapy. [Mh] Termos MeSH primário: Adipócitos/efeitos dos fármacos Inibidores Enzimáticos/farmacologia Transição Epitelial-Mesenquimal/efeitos dos fármacos Quinase 3 da Glicogênio Sintase/genética Células Mesenquimais Estromais/efeitos dos fármacos Fator de Crescimento Transformador beta1/genética Proteínas de Xenopus/genética [Mh] Termos MeSH secundário: Adipócitos/citologia Adipócitos/metabolismo Tecido Adiposo/citologia Tecido Adiposo/efeitos dos fármacos Tecido Adiposo/metabolismo Caderinas/genética Caderinas/metabolismo Movimento Celular/efeitos dos fármacos Molécula de Adesão da Célula Epitelial/genética Molécula de Adesão da Célula Epitelial/metabolismo Regulação da Expressão Gênica Quinase 3 da Glicogênio Sintase/antagonistas & inibidores Quinase 3 da Glicogênio Sintase/metabolismo Seres Humanos Integrina alfa5/genética Integrina alfa5/metabolismo Células Mesenquimais Estromais/citologia Células Mesenquimais Estromais/metabolismo Ocludina/genética Ocludina/metabolismo Cultura Primária de Células Pirazóis/farmacologia Piridinas/farmacologia Pirimidinas/farmacologia Fatores de Transcrição da Família Snail/genética Fatores de Transcrição da Família Snail/metabolismo Tiossemicarbazonas/farmacologia Fator de Crescimento Transformador beta1/antagonistas & inibidores Fator de Crescimento Transformador beta1/metabolismo Tranilcipromina/farmacologia Tretinoína/farmacologia Ácido Valproico/farmacologia Vimentina/genética Vimentina/metabolismo Proteínas de Xenopus/antagonistas & inibidores Proteínas de Xenopus/metabolismo Homeobox 1 de Ligação a E-box em Dedo de Zinco/genética Homeobox 1 de Ligação a E-box em Dedo de Zinco/metabolismo Proteína da Zônula de Oclusão-1/genética Proteína da Zônula de Oclusão-1/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (A-83-01); 0 (CDH1 protein, human); 0 (Cadherins); 0 (Chir 99021); 0 (EPCAM protein, human); 0 (Enzyme Inhibitors); 0 (Epithelial Cell Adhesion Molecule); 0 (Integrin alpha5); 0 (OCLN protein, human); 0 (Occludin); 0 (Pyrazoles); 0 (Pyridines); 0 (Pyrimidines); 0 (RepSox); 0 (SNAI1 protein, human); 0 (Snail Family Transcription Factors); 0 (TJP1 protein, human); 0 (Thiosemicarbazones); 0 (Transforming Growth Factor beta1); 0 (Vimentin); 0 (Xenopus Proteins); 0 (ZEB1 protein, human); 0 (Zinc Finger E-box-Binding Homeobox 1); 0 (Zonula Occludens-1 Protein); 3E3V44J4Z9 (Tranylcypromine); 5688UTC01R (Tretinoin); 614OI1Z5WI (Valproic Acid); EC 2.7.11.26 (GSK3 protein, Xenopus); EC 2.7.11.26 (Glycogen Synthase Kinase 3) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 170808 [Lr] Data última revisão: 170808 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170713 [St] Status: MEDLINE

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[PMID]: 28381189 [Au] Autor: Chuanyu S; Yuqing Z; Chong X; Guowei X; Xiaojun Z [Ad] Endereço: 1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, China. [Ti] Título: Periostin promotes migration and invasion of renal cell carcinoma through the integrin/focal adhesion kinase/c-Jun N-terminal kinase pathway. [So] Source: Tumour Biol;39(4):1010428317694549, 2017 Apr. [Is] ISSN: 1423-0380 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Periostin (POSTN) is an extracellular matrix protein which is overexpressed in a variety of cancers and has been related to tumorigenesis of renal cell carcinoma. However, the involvement of POSTN in renal cell carcinoma migration, invasion, and their underlying mechanisms has not been established. In this study, renal cell carcinoma cell lines stably overexpressing POSTN were established using a lentiviral vector, and the effects of POSTN on renal cell carcinoma cell migration and invasion were investigated. POSTN overexpression increased the migration and invasion capabilities of renal cell carcinoma cell lines as well as activity of matrix metalloproteinase-2 and matrix metalloproteinase-9. Integrin α ß and α ß antibodies inhibited POSTN overexpression or recombinant POSTN-induced focal adhesion kinase activation, cell migration, and invasion. Furthermore, lentivirus-mediated focal adhesion kinase knockdown and c-Jun N-terminal kinase inhibitor reduced POSTN-enhanced phosphorylation of c-Jun N-terminal kinase, matrix metalloproteinase-9 and matrix metalloproteinase-2 expressions, cell migration, and invasion. Our research thus indicates that POSTN promotes renal cell carcinoma cell migration and invasion through interaction with integrins α ß and α ß and subsequent activation of the focal adhesion kinase/c-Jun N-terminal kinase pathway. These results suggest that POSTN plays a critical role in renal cell carcinoma metastasis and may represent a potential target for novel therapeutic approaches against renal cell carcinoma. [Mh] Termos MeSH primário: Carcinoma de Células Renais/patologia Moléculas de Adesão Celular/fisiologia Movimento Celular Proteína-Tirosina Quinases de Adesão Focal/fisiologia Proteínas Quinases JNK Ativadas por Mitógeno/fisiologia Neoplasias Renais/patologia Sistema de Sinalização das MAP Quinases [Mh] Termos MeSH secundário: Linhagem Celular Tumoral Seres Humanos Integrina alfa5/fisiologia Invasividade Neoplásica [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Cell Adhesion Molecules); 0 (Integrin alpha5); 0 (POSTN protein, human); EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases) [Em] Mês de entrada: 1704 [Cu] Atualização por classe: 170418 [Lr] Data última revisão: 170418 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170407 [St] Status: MEDLINE [do] DOI: 10.1177/1010428317694549

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[PMID]: 28356422 [Au] Autor: Starchenko A; Graves-Deal R; Yang YP; Li C; Zent R; Singh B; Coffey RJ [Ad] Endereço: Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37232. [Ti] Título: Clustering of integrin α5 at the lateral membrane restores epithelial polarity in invasive colorectal cancer cells. [So] Source: Mol Biol Cell;28(10):1288-1300, 2017 May 15. [Is] ISSN: 1939-4586 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Apicobasolateral polarity is a fundamental property of epithelial cells, and its loss is a hallmark of cancer. Integrin-mediated contact with the extracellular matrix defines the basal surface, setting in motion E-cadherin-mediated cell-cell contact, which establishes apicobasolateral polarity. Role(s) for lateral integrins in this polarization process and the consequences of their disruption are incompletely understood. We show that addition of an integrin ß1-activating monoclonal antibody, P4G11, to invasive colorectal cancer cells in three-dimensional type 1 collagen reverts the invasive phenotype and restores apicobasolateral polarity. P4G11 induces clustering of integrin α5ß1 at lateral, intercellular surfaces. This leads to deposition and polymerization of fibronectin and recruitment of paxillin to sites of lateral integrin α5ß1 clustering and is followed by tight junction formation, as determined by ZO-1 localization. Inducible elimination of integrin α5 abrogates the epithelial-organizing effects of P4G11. In addition, polymerization of fibronectin is required for the effects of P4G11, and addition of polymerized superfibronectin is sufficient to induce tight junction formation and apicobasolateral polarization. In the normal human colon, we show that integrin α5 localizes to the lateral membrane of terminally differentiated colonocytes and that integrin α5 staining may be reduced in colorectal cancer. Thus we propose a novel role for integrin α5ß1 in regulating epithelial morphogenesis. [Mh] Termos MeSH primário: Integrina alfa5beta1/metabolismo [Mh] Termos MeSH secundário: Anticorpos Caderinas Adesão Celular/fisiologia Técnicas de Cultura de Células Linhagem Celular Tumoral Polaridade Celular/fisiologia Neoplasias Colorretais/metabolismo Células Epiteliais/metabolismo Células Epiteliais/fisiologia Matriz Extracelular/metabolismo Fibronectinas/metabolismo Seres Humanos Integrina alfa5/metabolismo Integrina alfa5/fisiologia Integrina alfa5beta1/fisiologia Integrina beta1/metabolismo Proteínas de Membrana Membranas/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antibodies); 0 (Cadherins); 0 (Fibronectins); 0 (Integrin alpha5); 0 (Integrin alpha5beta1); 0 (Integrin beta1); 0 (Membrane Proteins) [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: 170331 [St] Status: MEDLINE [do] DOI: 10.1091/mbc.E16-12-0852

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[PMID]: 28179307 [Au] Autor: Ryu SH; Heo SH; Park EY; Choi KC; Ryu JW; Lee SH; Lee SW [Ad] Endereço: Department of Radiation Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea. [Ti] Título: Selumetinib Inhibits Melanoma Metastasis to Mouse Liver Suppression of EMT-targeted Genes. [So] Source: Anticancer Res;37(2):607-614, 2017 02. [Is] ISSN: 1791-7530 [Cp] País de publicação: Greece [La] Idioma: eng [Ab] Resumo: AIM: We investigated the therapeutic effects of a mitogen-activated protein (MEK) inhibitor, selumetinib, in a hepatic melanoma metastasis model and studied its possible mechanism of action. MATERIALS AND METHODS: Melanoma cell lines were exposed to selumetinib under different experimental conditions. We established a mouse model of liver metastasis and treated mice orally with vehicle or selumetinib and then evaluated metastasis progress. RESULTS: Growth inhibition was observed in melanoma cells as a consequence of G -phase cell-cycle arrest and the subsequent induction of apoptosis in a dose- and time-dependent manner. Mice with established liver metastases that were treated with selumetinib exhibited significantly less tumor progression than vehicle-treated mice. c-Myc expression in metastasized liver tissues were suppressed by selumetinib. Moreover, oral treatment with selumetinib modulated expression of epithelial-to-mesenchymal transition- and metastasis-related genes, including integrin alpha-5 (ITGA5), jagged 1 (JAG1), zinc finger E-box-binding homeobox 1 (ZEB1), NOTCH, and serpin peptidase inhibitor clade E (SERPINE1). CONCLUSION: We established a mouse model of hepatic metastasis using a human melanoma cell line, such models are essential in elucidating the therapeutic effects of anti-metastatic drugs. Our data suggest the possibility that selumetinib presents a new strategy to treat liver metastasis in patients with melanoma by suppressing epithelial-to-mesenchymal transition-related genes. [Mh] Termos MeSH primário: Benzimidazóis/farmacologia Transição Epitelial-Mesenquimal/efeitos dos fármacos Neoplasias Hepáticas/prevenção & controle Melanoma/tratamento farmacológico [Mh] Termos MeSH secundário: Administração Oral Animais Apoptose/efeitos dos fármacos Apoptose/genética Benzimidazóis/administração & dosagem Linhagem Celular Tumoral Proliferação Celular/efeitos dos fármacos Proliferação Celular/genética Transição Epitelial-Mesenquimal/genética Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos Pontos de Checagem da Fase G1 do Ciclo Celular/genética Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos Seres Humanos Immunoblotting Integrina alfa5/genética Integrina alfa5/metabolismo Proteína Jagged-1/genética Proteína Jagged-1/metabolismo Neoplasias Hepáticas/genética Neoplasias Hepáticas/secundário Masculino Melanoma/genética Melanoma/patologia Camundongos Endogâmicos BALB C Camundongos Nus Reação em Cadeia da Polimerase Via Transcriptase Reversa Fator de Crescimento Transformador beta1/genética Fator de Crescimento Transformador beta1/metabolismo Ensaios Antitumorais Modelo de Xenoenxerto [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (AZD 6244); 0 (Benzimidazoles); 0 (Integrin alpha5); 0 (JAG1 protein, human); 0 (Jagged-1 Protein); 0 (Transforming Growth Factor beta1) [Em] Mês de entrada: 1702 [Cu] Atualização por classe: 170227 [Lr] Data última revisão: 170227 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170210 [St] Status: MEDLINE

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[PMID]: 28131812 [Au] Autor: Villegas-Pineda JC; Toledo-Leyva A; Osorio-Trujillo JC; Hernández-Ramírez VI; Talamás-Rohana P [Ad] Endereço: Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Av. Instituto Politécnico Nacional 2508, Col. San Pedro Zacatenco, Delegación Gustavo A. Madero, Ciudad de México 07360, Mexico. Electronic address: jcvillegas@cin [Ti] Título: The translational blocking of α5 and α6 integrin subunits affects migration and invasion, and increases sensitivity to carboplatin of SKOV-3 ovarian cancer cell line. [So] Source: Exp Cell Res;351(2):127-134, 2017 Feb 15. [Is] ISSN: 1090-2422 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Epithelial ovarian cancer is the most lethal gynecologic malignancy. Integrins, overexpressed in cancer, are involved in various processes that favor the development of the disease. This study focused on determining the degree of involvement of α5, α6 and ß3 integrin subunits in the establishment/development of epithelial ovarian cancer (EOC), such as proliferation, migration, invasion, and response to carboplatin. The translation of the α5, α6 and ß3 integrins was blocked using morpholines, generating morphant cells for these proteins, which were corroborated by immunofluorescence assays. WST-1 proliferation assay showed that silencing of α5, α6, and ß3 integrins does not affect the survival of morphants. Wound healing and transwell chamber assays showed that blocking α5 and α6 integrins decrease, in lesser and greater level respectively, the migratory and the invasive capacity of SKOV-3 cells. Finally, blocking α5 and α6 integrins partially sensitized the cells response to carboplatin, while blocking integrin ß3 generated resistance to this drug. Statistical analyses were performed with the GraphPad Prism 5.0 software employing one way and two-way ANOVA tests; data are shown as average±SD. Results suggest that α5 and α6 integrins could become good candidates for chemotherapy targets in EOC. [Mh] Termos MeSH primário: Antineoplásicos/farmacologia Carboplatina/farmacologia Regulação Neoplásica da Expressão Gênica Integrina alfa5/genética Integrina alfa6/genética Morfolinas/farmacologia Biossíntese de Proteínas/efeitos dos fármacos [Mh] Termos MeSH secundário: Linhagem Celular Tumoral Movimento Celular/efeitos dos fármacos Cultura em Câmaras de Difusão Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos Resistência a Medicamentos Antineoplásicos/genética Células Epiteliais/efeitos dos fármacos Células Epiteliais/metabolismo Células Epiteliais/patologia Feminino Seres Humanos Integrina alfa5/metabolismo Integrina alfa6/metabolismo Integrina beta3/genética Integrina beta3/metabolismo Ovário/efeitos dos fármacos Ovário/metabolismo Ovário/patologia Transdução de Sinais [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (Integrin alpha5); 0 (Integrin alpha6); 0 (Integrin beta3); 0 (Morpholines); BG3F62OND5 (Carboplatin) [Em] Mês de entrada: 1705 [Cu] Atualização por classe: 170518 [Lr] Data última revisão: 170518 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170130 [St] Status: MEDLINE

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[PMID]: 28107390 [Au] Autor: Nikolovska K; Spillmann D; Haier J; Ladányi A; Stock C; Seidler DG [Ad] Endereço: Institute of Physiological Chemistry and Pathobiochemistry, University of Münster, Münster, Germany. [Ti] Título: Melanoma Cell Adhesion and Migration Is Modulated by the Uronyl 2-O Sulfotransferase. [So] Source: PLoS One;12(1):e0170054, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Although the vast majority of melanomas are characterized by a high metastatic potential, if detected early, melanoma can have a good prognostic outcome. However, once metastasised, the prognosis is bleak. We showed previously that uronyl-2-O sulfotransferase (Ust) and 2-O sulfation of chondroitin/dermatan sulfate (CS/DS) are involved in cell migration. To demonstrate an impact of 2-O sulfation in metastasis we knocked-down Ust in mouse melanoma cells. This significantly reduced the amount of Ust protein and enzyme activity. Furthermore, in vitro cell motility and adhesion were significantly reduced correlating with the decrease of cellular Ust protein. Single cell migration of B16VshUst(16) cells showed a decreased cell movement phenotype. The adhesion of B16V cells to fibronectin depended on α5ß1 but not αvß3 integrin. Inhibition of glycosaminoglycan sulfation or blocking fibroblast growth factor receptor (FgfR) reduced α5 integrin in B16V cell lines. Interestingly, FgfR1 expression and activation was reduced in Ust knock-down cells. In vivo, pulmonary metastasis of B16VshUst cells was prevented due to a reduction of α5 integrin. As a proof of concept UST knock-down in human melanoma cells also showed a reduction in ITGa5 and adhesion. This is the first study showing that Ust, and consequently 2-O sulfation of the low affinity receptor for FgfR CS/DS, reduces Itga5 and leads to an impaired adhesion and migration of melanoma cells. [Mh] Termos MeSH primário: Neoplasias Pulmonares/secundário Melanoma Experimental/patologia Sulfotransferases/metabolismo [Mh] Termos MeSH secundário: Animais Linhagem Celular Tumoral Inativação Gênica Integrina alfa5/genética Camundongos Camundongos Knockout Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/genética Sulfotransferases/genética [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Integrin alpha5); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1); EC 2.8.2.- (Sulfotransferases); EC 2.8.2.- (uronyl 2-O-sulfotransferase, mouse) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 170810 [Lr] Data última revisão: 170810 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170121 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0170054

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[PMID]: 28093522 [Au] Autor: Aw Yeang HX; Piersma SJ; Lin Y; Yang L; Malkova ON; Miner C; Krupnick AS; Chapman WC; Yokoyama WM [Ad] Endereço: Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110. [Ti] Título: Cutting Edge: Human CD49e- NK Cells Are Tissue Resident in the Liver. [So] Source: J Immunol;198(4):1417-1422, 2017 Feb 15. [Is] ISSN: 1550-6606 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Most knowledge on NK cells is based on studies of what are now known as conventional NK cells in the mouse spleen or human peripheral blood. However, recent studies in mice indicate the presence of tissue-resident NK cells in certain organs, such as the liver, that display different markers and transcription factor dependencies as compared with conventional NK cells. In this study, we provide evidence from cytometry by time-of-flight analysis and humanized mice indicating that human CD49e NK cells are tissue resident in the liver. Thus, these studies indicate that tissue-resident NK cells are evolutionarily conserved in humans and mice, providing a foundation to explore their role in human disease. [Mh] Termos MeSH primário: Integrina alfa5/imunologia Células Matadoras Naturais/fisiologia Fígado/citologia Fígado/imunologia [Mh] Termos MeSH secundário: Animais Capilares/imunologia Citometria de Fluxo Seres Humanos Integrina alfa5/genética Células Matadoras Naturais/imunologia Fígado/irrigação sanguínea Camundongos Camundongos Transgênicos Fenótipo Fatores de Transcrição [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Integrin alpha5); 0 (Transcription Factors) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 170922 [Lr] Data última revisão: 170922 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 170118 [St] Status: MEDLINE [do] DOI: 10.4049/jimmunol.1601818

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[PMID]: 28073834 [Au] Autor: Kim HJ; Kwon S; Nam SH; Jung JW; Kang M; Ryu J; Kim JE; Cheong JG; Cho CY; Kim S; Song DG; Kim YN; Kim TY; Jung MK; Lee KM; Pack CG; Lee JW [Ad] Endereço: Department of Pharmacy, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, South Korea. [Ti] Título: Dynamic and coordinated single-molecular interactions at TM4SF5-enriched microdomains guide invasive behaviors in 2- and 3-dimensional environments. [So] Source: FASEB J;31(4):1461-1481, 2017 Apr. [Is] ISSN: 1530-6860 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Membrane proteins sense extracellular cues and transduce intracellular signaling to coordinate directionality and speed during cellular migration. They are often localized to specific regions, as with lipid rafts or tetraspanin-enriched microdomains; however, the dynamic interactions of tetraspanins with diverse receptors within tetraspanin-enriched microdomains on cellular surfaces remain largely unexplored. Here, we investigated effects of tetraspan(in) TM4SF5 (transmembrane 4 L6 family member 5)-enriched microdomains (T ERMs) on the directionality of cell migration. Physical association of TM4SF5 with epidermal growth factor receptor (EGFR) and integrin α5 was visualized by live fluorescence cross-correlation spectroscopy and higher-resolution microscopy at the leading edge of migratory cells, presumably forming TM4SF5-enriched microdomains. Whereas TM4SF5 and EGFR colocalized at the migrating leading region more than at the rear, TM4SF5 and integrin α5 colocalized evenly throughout cells. Cholesterol depletion and disruption in TM4SF5 post-translational modifications, including -glycosylation and palmitoylation, altered TM4SF5 interactions and cellular localization, which led to less cellular migration speed and directionality in 2- or 3-dimensional conditions. TM4SF5 controlled directional cell migration and invasion, and importantly, these TM4SF5 functions were dependent on cholesterol, TM4SF5 post-translational modifications, and EGFR and integrin α5 activity. Altogether, we showed that TM4SF5 dynamically interacted with EGFR and integrin α5 in migratory cells to control directionality and invasion.-Kim, H.-J., Kwon, S., Nam, S. H., Jung, J. W., Kang, M., Ryu, J., Kim, J. E., Cheong, J.-G., Cho, C. Y., Kim, S., Song, D.-G., Kim, Y.-N., Kim, T. Y., Jung, M.-K., Lee, K.-M., Pack, C.-G., Lee, J. W. Dynamic and coordinated single-molecular interactions at TM4SF5-enriched microdomains guide invasive behaviors in 2- and 3-dimensional environments. [Mh] Termos MeSH primário: Microdomínios da Membrana/metabolismo Proteínas de Membrana/metabolismo [Mh] Termos MeSH secundário: Linhagem Celular Tumoral Movimento Celular Colesterol/metabolismo Glicosilação Células HEK293 Hepatócitos/metabolismo Hepatócitos/fisiologia Hepatócitos/ultraestrutura Seres Humanos Integrina alfa5/metabolismo Lipoilação Microdomínios da Membrana/ultraestrutura Ligação Proteica Processamento de Proteína Pós-Traducional Receptor do Fator de Crescimento Epidérmico/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Integrin alpha5); 0 (Membrane Proteins); 0 (TM4SF5 protein, human); 97C5T2UQ7J (Cholesterol); EC 2.7.10.1 (Receptor, Epidermal Growth Factor) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170906 [Lr] Data última revisão: 170906 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170112 [St] Status: MEDLINE [do] DOI: 10.1096/fj.201600944RR

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[PMID]: 27808427 [Au] Autor: Hu P; Luo BH [Ad] Endereço: Department of Biological Sciences, Louisiana State University, Baton Rouge, Louisiana. [Ti] Título: Integrin α ß Adopts a High Affinity State for Soluble Ligands Under Physiological Conditions. [So] Source: J Cell Biochem;118(8):2044-2052, 2017 Aug. [Is] ISSN: 1097-4644 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: It has been proposed that integrins adopt a low affinity conformation under physiological conditions. Integrin can either be activated through cytoplasm or by binding of cations such as Mn to the head domain. The cytoplasmic activation pathway, that is, inside-out signaling has been regarded as the physiological pathway for integrin activation. Integrin ß is important for neuron vascular development. However, due to the highly divergent cytoplasmic domain, this integrin probably does not rely on inside-out signaling for affinity regulation. We therefore hypothesized that the ß integrin uniquely assumes a constitutively high affinity state under physiological conditions. We discovered that ß indeed exhibited high binding to soluble vitronectin in the presence of Ca and the ligand binding could not be further enhanced by addition of Mn . The lower ectodomain stalk of the integrin, which is comprised by the integrin epidermal growth factor-like (I-EGF) domains and ßTD domain, is critical for this high affinity conformation. In addition, we found that unlike other integrins, Mg at low concentration inhibited ß ligand binding. Mutagenesis studies indicated that ß integrin possesses a unique cation binding site which might contribute to the ligand binding affinity. Our study showed that both the ß lower ectodomain stalk and the head domain play an important role in its high affinity state under physiological conditions. J. Cell. Biochem. 118: 2044-2052, 2017. © 2016 Wiley Periodicals, Inc. [Mh] Termos MeSH primário: Cálcio/química Integrina alfa5/química Cadeias beta de Integrinas/química Proteínas Recombinantes de Fusão/química Vitronectina/química [Mh] Termos MeSH secundário: Sequência de Aminoácidos Sítios de Ligação Cálcio/metabolismo Cátions Bivalentes Expressão Gênica Células HEK293 Seres Humanos Integrina alfa5/genética Integrina alfa5/metabolismo Cadeias beta de Integrinas/genética Cadeias beta de Integrinas/metabolismo Ligantes Magnésio/química Magnésio/metabolismo Manganês/química Manganês/metabolismo Mutação Ligação Proteica Domínios Proteicos Proteínas Recombinantes de Fusão/genética Proteínas Recombinantes de Fusão/metabolismo Alinhamento de Sequência Homologia de Sequência de Aminoácidos Solubilidade Soluções Vitronectina/genética Vitronectina/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Cations, Divalent); 0 (Integrin alpha5); 0 (Integrin beta Chains); 0 (Ligands); 0 (Recombinant Fusion Proteins); 0 (Solutions); 0 (Vitronectin); 0 (integrin beta8); 42Z2K6ZL8P (Manganese); I38ZP9992A (Magnesium); SY7Q814VUP (Calcium) [Em] Mês de entrada: 1711 [Cu] Atualização por classe: 171102 [Lr] Data última revisão: 171102 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 161104 [St] Status: MEDLINE [do] DOI: 10.1002/jcb.25780

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MEDLINE

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[PMID]: 27599164 [Au] Autor: Singh R; Hui T; Matsui A; Allahem Z; Johnston CD; Ruiz-Torruella M; Rittling SR [Ad] Endereço: Department of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA. [Ti] Título: Modulation of infection-mediated migration of neutrophils and CXCR2 trafficking by osteopontin. [So] Source: Immunology;150(1):74-86, 2017 Jan. [Is] ISSN: 1365-2567 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Osteopontin (OPN) is a pro-inflammatory protein that paradoxically protects against inflammation and bone destruction in a mouse model of endodontic infection. Here we have tested the hypothesis that this effect of OPN is mediated by effects on migration of innate immune cells to the site of infection. Using the air pouch as a model of endodontic infection in mice, we showed that neutrophil accumulation at the site of infection with a mixture of endodontic pathogens is significantly reduced in OPN-deficient mice. Reduced neutrophil accumulation in the absence of OPN was accompanied by an increase in bacterial load. OPN-deficiency did not affect neutrophil survival, CXCR2 ligand expression, or the production of inflammatory cytokines in the air pouch. In vitro, OPN enhanced neutrophil migration to CXCL1, whereas in vivo, inhibition of CXCR2 suppressed cellular infiltration in air pouches of infected wild-type mice by > 50%, but had no effect in OPN-deficient mice. OPN increased cell surface expression of CXCR2 on bone marrow neutrophils in an integrin-α -dependent manner, and suppressed the internalization of CXCR2 in the absence of ligand. Together, these results support a model where the protective effect of OPN results from enhanced initial neutrophil accumulation at sites of infection resulting in optimal bacterial killing. We describe a novel mechanism for this effect of OPN: integrin-α -dependent suppression of CXCR2 internalization in neutrophils, which increases the ability of these cells to migrate to sites of infection in response to CXCR2 ligands. [Mh] Termos MeSH primário: Infecções Bacterianas/imunologia Integrina alfa5/metabolismo Neutrófilos/imunologia Osteopontina/metabolismo Pulpite/imunologia [Mh] Termos MeSH secundário: Animais Carga Bacteriana Movimento Celular Quimiocina CXCL1/metabolismo Modelos Animais de Doenças Seres Humanos Imunidade Inata/genética Integrina alfa5/genética Masculino Camundongos Camundongos da Linhagem 129 Camundongos Endogâmicos C57BL Camundongos Knockout Osteopontina/genética Receptores de Interleucina-8B/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Chemokine CXCL1); 0 (Integrin alpha5); 0 (Receptors, Interleukin-8B); 106441-73-0 (Osteopontin) [Em] Mês de entrada: 1705 [Cu] Atualização por classe: 170523 [Lr] Data última revisão: 170523 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160907 [St] Status: MEDLINE [do] DOI: 10.1111/imm.12668

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