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Pesquisa : G05.360.340.024.340.375.500.791.570 [Categoria DeCS]
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[PMID]:28417908
[Au] Autor:Nakayama Y; Soeda S; Ikeuchi M; Kakae K; Yamaguchi N
[Ad] Endereço:Department of Biochemistry & Molecular Biology, Kyoto Pharmaceutical University, Kyoto 607-8414, Japan. nakayama@mb.kyoto-phu.ac.jp.
[Ti] Título:Cytokinesis Failure Leading to Chromosome Instability in v-Src-Induced Oncogenesis.
[So] Source:Int J Mol Sci;18(4), 2017 Apr 12.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:v-Src, an oncogene found in Rous sarcoma virus, is a constitutively active variant of c-Src. Activation of Src is observed frequently in colorectal and breast cancers, and is critical in tumor progression through multiple processes. However, in some experimental conditions, v-Src causes growth suppression and apoptosis. In this review, we highlight recent progress in our understanding of cytokinesis failure and the attenuation of the tetraploidy checkpoint in v-Src-expressing cells. v-Src induces cell cycle changes-such as the accumulation of the 4N cell population-and increases the number of binucleated cells, which is accompanied by an excess number of centrosomes. Time-lapse analysis of v-Src-expressing cells showed that cytokinesis failure is caused by cleavage furrow regression. Microscopic analysis revealed that v-Src induces delocalization of cytokinesis regulators including Aurora B and Mklp1. Tetraploid cell formation is one of the causes of chromosome instability; however, tetraploid cells can be eliminated at the tetraploidy checkpoint. Interestingly, v-Src weakens the tetraploidy checkpoint by inhibiting the nuclear exclusion of the transcription coactivator YAP, which is downstream of the Hippo pathway and its nuclear exclusion is critical in the tetraploidy checkpoint. We also discuss the relationship between v-Src-induced chromosome instability and growth suppression in v-Src-induced oncogenesis.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/genética
Instabilidade Cromossômica
Citocinese/genética
Genes src
[Mh] Termos MeSH secundário: Animais
Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Proliferação Celular/genética
Variação Genética
Seres Humanos
Mitose/genética
Transporte Proteico
Tetraploidia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cell Cycle Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE


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[PMID]:28286042
[Au] Autor:Chen L; Li J; Ke X; Qu W; Zhang J; Feng F; Liu W
[Ad] Endereço:Department of Pharmaceutical Analysis, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing 210009, China.
[Ti] Título:The therapeutic effects of Periploca forrestii Schltr. Stem extracts on collagen-induced arthritis by inhibiting the activation of Src/NF-κB signaling pathway in rats.
[So] Source:J Ethnopharmacol;202:12-19, 2017 Apr 18.
[Is] ISSN:1872-7573
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:ETHNOPHARMACOLOGICAL RELEVANCE: Periploca forrestii Schltr. is a classical traditional Chinese medicine (TCM) called Heilonggu (HLG) in China. According to the theory of TCM, it possesses the efficacy of eliminating wind and removing dampness. In clinical practice, it is commonly used for the treatment of rheumatoid arthritis. The present work aimed to evaluate the anti-rheumatism activity of HLG ethanol extract and reveal the underlying molecular mechanism by employing an animal model of collagen-induced rheumatoid arthritis (CIA) in rats. MATERIALS AND METHODS: The CIA was induced in male Sprague-Dawley rats by intradermal injection of bovine collagen-II in complete Freund's adjuvant (CFA) at the base of tail. The rats received oral administration of HLG (200 and 400mg/kg) from day 1, with the treatment lasting for 28 days. A variety of indicators were measured for evaluation of anti-rheumatism effect, including paw swelling, arthritis scores, and histopathological changes. Furthermore, the serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and prostaglandin E2 (PGE2), as well as cyclooxygenase-2 (COX-2), nuclear factor NF-κB p65 and Src kinase in joint synovial tissues were detected to explore the possible mechanisms. RESULTS: The administration of HLG significantly restored type II collagen-induced arthritis in rats as evidenced by decrease in paw swelling and inflammatory factors in serum. Meanwhile, this treatment also notably reduced NF-κB p65 and COX-2 expression. Surprisingly, the activity of Src kinase was also inhibited demonstrated by downregulation of phosphorylated Src. CONCLUSION: Our results revealed that HLG possessed observable therapeutic action on collagen-induced arthritis by inhibiting the activation of Src and nuclear translocation of NF-κB in rats. HLG may serve as a potential candidate for the management of patients with RA.
[Mh] Termos MeSH primário: Artrite Experimental/tratamento farmacológico
Genes src/efeitos dos fármacos
NF-kappa B/efeitos dos fármacos
Periploca
Extratos Vegetais/uso terapêutico
Caules de Planta/química
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/patologia
Dinoprostona/metabolismo
Interleucina-6/metabolismo
Articulações/metabolismo
Articulações/patologia
Masculino
Periploca/química
Periploca/toxicidade
Extratos Vegetais/toxicidade
Caules de Planta/toxicidade
Ratos
Ratos Sprague-Dawley
Membrana Sinovial/metabolismo
Membrana Sinovial/patologia
Fator de Transcrição RelA/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-6); 0 (NF-kappa B); 0 (Plant Extracts); 0 (Transcription Factor RelA); 0 (Tumor Necrosis Factor-alpha); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE


  3 / 928 MEDLINE  
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[PMID]:28223314
[Au] Autor:González L; Miquet JG; Irene PE; Díaz ME; Rossi SP; Sotelo AI; Frungieri MB; Hill CM; Bartke A; Turyn D
[Ad] Endereço:Instituto de Química y Fisicoquímica Biológicas (UBA-CONICET)Facultad de Farmacia y Bioquímica, Buenos Aires, Argentina lgonzalez@qb.ffyb.uba.ar.
[Ti] Título:Attenuation of epidermal growth factor (EGF) signaling by growth hormone (GH).
[So] Source:J Endocrinol;233(2):175-186, 2017 May.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Transgenic mice overexpressing growth hormone (GH) show increased hepatic protein content of the epidermal growth factor receptor (EGFR), which is broadly associated with cell proliferation and oncogenesis. However, chronically elevated levels of GH result in desensitization of STAT-mediated EGF signal and similar response of ERK1/2 and AKT signaling to EGF compared to normal mice. To ascertain the mechanisms involved in GH attenuation of EGF signaling and the consequences on cell cycle promotion, phosphorylation of signaling mediators was studied at different time points after EGF stimulation, and induction of proteins involved in cell cycle progression was assessed in normal and GH-overexpressing transgenic mice. Results from kinetic studies confirmed the absence of STAT3 and 5 activation and comparable levels of ERK1/2 phosphorylation upon EGF stimulation, which was associated with diminished or similar induction of c-MYC, c-FOS, c-JUN, CYCLIN D1 and CYCLIN E in transgenic compared to normal mice. Accordingly, kinetics of EGF-induced c-SRC and EGFR phosphorylation at activating residues demonstrated that activation of these proteins was lower in the transgenic mice with respect to normal animals. In turn, EGFR phosphorylation at serine 1046/1047, which is implicated in the negative regulation of the receptor, was increased in the liver of GH-overexpressing transgenic mice both in basal conditions and upon EGF stimulus. Increased basal phosphorylation and activation of the p38-mitogen-activated protein kinase might account for increased Ser 1046/1047 EGFR. Hyperphosphorylation of EGFR at serine residues would represent a compensatory mechanism triggered by chronically elevated levels of GH to mitigate the proliferative response induced by EGF.
[Mh] Termos MeSH primário: Fator de Crescimento Epidérmico/farmacologia
Regulação da Expressão Gênica/fisiologia
Hormônio do Crescimento/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Animais
MAP Quinases Reguladas por Sinal Extracelular/genética
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Genes src/genética
Genes src/fisiologia
Hormônio do Crescimento/genética
Seres Humanos
Fígado/metabolismo
Camundongos
Camundongos Transgênicos
Receptor do Fator de Crescimento Epidérmico/genética
Receptor do Fator de Crescimento Epidérmico/metabolismo
Fatores de Transcrição STAT/genética
Fatores de Transcrição STAT/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/genética
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (STAT Transcription Factors); 62229-50-9 (Epidermal Growth Factor); 9002-72-6 (Growth Hormone); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-16-0606


  4 / 928 MEDLINE  
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[PMID]:28085008
[Au] Autor:Huang K; Chen J; Yang MS; Tang YJ; Pan F
[Ti] Título:Inhibition of Src by microRNA-23b increases the cisplatin sensitivity of chondrosarcoma cells.
[So] Source:Cancer Biomark;18(3):231-239, 2017.
[Is] ISSN:1875-8592
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chondrosarcomas are malignant cartilage-forming tumors from low-grade to high-grade aggressive tumors characterized by metastasis. Cisplatin is an effective DNA-damaging anti-tumor agent for the treatment against a wide variety of solid tumors. However, chondrosarcomas are notorious for their resistance to conventional chemo- and radio- therapies. In this study, we report miR-23b acts as a tumor suppressor in chondrosarcoma. The expressions of miR-23b are down-regulated in chondrosarcoma patient samples and cell lines compared with adjacent normal tissues and human primary chondrocytes. In addition, overexpression of miR-23b suppresses chondrosarcoma cell proliferation. By comparison of the cisplatin resistant chondrosarcoma cells and parental cells, we observed miR-23b was significantly down regulated in cisplatin resistant cells. Moreover, we demonstrate here Src kinase is a direct target of miR-23b in chondrosarcoma cells. Overexpression of miR-23b suppresses Src-Akt pathway, leading to the sensitization of cisplatin resistant chondrosarcoma cells to cisplatin. This chemo-sensitivity effect by the miR-23b-mediated inhibition of Src-Akt pathway is verified with the restoration of Src kinase in miR-23b-overespressing chondrosarcoma cells, resulting in the acquirement of resistance to cisplatin. In summary, our study reveals a novel role of miR-23b in cisplatin resistance in chondrosarcoma and will contribute to the development of the microRNA-targeted anti-cancer therapeutics.
[Mh] Termos MeSH primário: Neoplasias Ósseas/genética
Condrossarcoma/genética
Cisplatino/farmacologia
Resistência a Medicamentos Antineoplásicos/genética
Genes src
MicroRNAs/genética
Interferência de RNA
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Sítios de Ligação
Neoplasias Ósseas/metabolismo
Linhagem Celular Tumoral
Condrossarcoma/metabolismo
Regulação Neoplásica da Expressão Gênica
Genes Supressores de Tumor
Seres Humanos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MIRN23 microRNA, human); 0 (MicroRNAs); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); Q20Q21Q62J (Cisplatin)
[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:170114
[St] Status:MEDLINE
[do] DOI:10.3233/CBM-160102


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[PMID]:27733622
[Au] Autor:Gottlieb-Abraham E; Gutman O; Pai GM; Rubio I; Henis YI
[Ad] Endereço:Department of Neurobiology, George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel.
[Ti] Título:The residue at position 5 of the N-terminal region of Src and Fyn modulates their myristoylation, palmitoylation, and membrane interactions.
[So] Source:Mol Biol Cell;27(24):3926-3936, 2016 Dec 01.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The interactions of Src family kinases (SFKs) with the plasma membrane are crucial for their activity. They depend on their fatty-acylated N-termini, containing N-myristate and either a polybasic cluster (in Src) or palmitoylation sites (e.g., Fyn). To investigate the roles of these moieties in SFK membrane association, we used fluorescence recovery after photobleaching beam-size analysis to study the membrane interactions of c-Src-GFP (green fluorescent protein) or Fyn-GFP fatty-acylation mutants. Our studies showed for the first time that the membrane association of Fyn is more stable than that of Src, an effect lost in a Fyn mutant lacking the palmitoylation sites. Unexpectedly, Src-S3C/S6C (containing cysteines at positions 3/6, which are palmitoylated in Fyn) exhibited fast cytoplasmic diffusion insensitive to palmitoylation inhibitors, suggesting defective fatty acylation. Further replacement of the charged Lys-5 by neutral Gln to resemble Fyn (Src-S3C/S6C/K5Q) restored Fyn-like membrane interactions, indicating that Lys-5 in the context of Src-S3C/S6C interferes with its myristoylation/palmitoylation. This was validated by direct myristoylation and palmitoylation studies, which indicated that the residue at position 5 regulates the membrane interactions of Src versus Fyn. Moreover, the palmitoylation levels correlated with targeting to detergent-resistant membranes (rafts) and to caveolin-1. Palmitoylation-dependent preferential containment of Fyn in rafts may contribute to its lower transformation potential.
[Mh] Termos MeSH primário: Genes src/genética
Genes src/fisiologia
Proteínas Proto-Oncogênicas c-fyn/metabolismo
[Mh] Termos MeSH secundário: Acilação
Sequência de Aminoácidos
Animais
Células COS
Caveolina 1/metabolismo
Membrana Celular/metabolismo
Cercopithecus aethiops
Cisteína/metabolismo
Proteínas de Fluorescência Verde
Lipoilação
Proteínas de Membrana
Membranas/metabolismo
Proteínas Proto-Oncogênicas/metabolismo
Proteínas Proto-Oncogênicas c-fyn/genética
Quinases da Família src/genética
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CAV1 protein, human); 0 (Caveolin 1); 0 (Membrane Proteins); 0 (Proto-Oncogene Proteins); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.10.2 (CSK tyrosine-protein kinase); EC 2.7.10.2 (FYN protein, human); EC 2.7.10.2 (Proto-Oncogene Proteins c-fyn); EC 2.7.10.2 (src-Family Kinases); K848JZ4886 (Cysteine)
[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:161014
[St] Status:MEDLINE


  6 / 928 MEDLINE  
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[PMID]:27439518
[Au] Autor:Gujar R; Maurya N; Yadav V; Gupta M; Arora S; Khatri N; Sen P
[Ad] Endereço:Division of Cell Biology and Immunology, Council of Scientific and Industrial Research-Institute of Microbial Technology, Chandigarh 160036, India; and.
[Ti] Título:c-Src Suppresses Dendritic Cell Antitumor Activity via T Cell Ig and Mucin Protein-3 Receptor.
[So] Source:J Immunol;197(5):1650-62, 2016 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The enhanced expression of T cell Ig and mucin protein-3 (TIM-3) on tumor-associated dendritic cells (DCs) attenuates antitumor effects of DNA vaccines. To identify a potential target (or targets) for reducing TIM-3 expression on tumor-associated DCs, we explored the molecular mechanisms regulating TIM-3 expression. In this study, we have identified a novel signaling pathway (c-Src→Bruton's tyrosine kinase→transcription factors Ets1, Ets2, USF1, and USF2) necessary for TIM-3 upregulation on DCs. Both IL-10 and TGF-ß, which are produced in the tumor microenvironment, upregulated TIM-3 expression on DCs via this pathway. Suppressed expression of c-Src or downstream Bruton's tyrosine kinase, Ets1, Ets2, USF1, or USF2 blocked IL-10- and TGF-ß-induced TIM-3 upregulation on DCs. Notably, in vivo knockdown of c-Src in mice reduced TIM-3 expression on tumor-associated DCs. Furthermore, adoptive transfer of c-Src-silenced DCs in mouse tumors enhanced the in vivo antitumor effects of immunostimulatory CpG DNA; however, TIM-3 overexpression in c-Src-silenced DCs blocked this effect. Collectively, our data reveal the molecular mechanism regulating TIM-3 expression in DCs and identify c-Src as a target for improving the efficacy of nucleic acid-mediated anticancer therapy.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Genes src
Receptor Celular 2 do Vírus da Hepatite A/metabolismo
Neoplasias/imunologia
Linfócitos T/imunologia
Quinases da Família src/metabolismo
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Diferenciação Celular
Regulação Neoplásica da Expressão Gênica
Técnicas de Silenciamento de Genes
Receptor Celular 2 do Vírus da Hepatite A/genética
Interleucina-10/imunologia
Interleucina-10/secreção
Camundongos
Neoplasias/metabolismo
Oligodesoxirribonucleotídeos/imunologia
Proteínas Tirosina Quinases/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fator de Crescimento Transformador beta/imunologia
Fator de Crescimento Transformador beta/secreção
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CPG-oligonucleotide); 0 (Havcr2 protein, mouse); 0 (Hepatitis A Virus Cellular Receptor 2); 0 (Oligodeoxyribonucleotides); 0 (Transforming Growth Factor beta); 130068-27-8 (Interleukin-10); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.2 (CSK tyrosine-protein kinase); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160722
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600104


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[PMID]:27108184
[Au] Autor:Stojanovic N; Brozovic A; Majhen D; Bosnar MH; Fritz G; Osmak M; Ambriovic-Ristov A
[Ad] Endereço:Laboratory for Cell Biology and Signalling, Division of Molecular Biology, Ruder Boskovic Institute, Bijenicka 54, 10000 Zagreb, Croatia.
[Ti] Título:Integrin αvß3 expression in tongue squamous carcinoma cells Cal27 confers anticancer drug resistance through loss of pSrc(Y418).
[So] Source:Biochim Biophys Acta;1863(8):1969-78, 2016 08.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Integrins play key roles in the regulation of tumor cell adhesion, migration, invasion and sensitivity to anticancer drugs. In the present study we investigate the mechanism of resistance of tongue squamous carcinoma cells Cal27 with de novo integrin αvß3 expression to anticancer drugs. Cal27-derived cell clones, obtained by transfection of plasmid containing integrin subunit ß3 cDNA, as compared to control cells demonstrate: expression of integrin αvß3; increased expression of integrin αvß5; increased adhesion to fibronectin and vitronectin; resistance to cisplatin, mitomycin C, doxorubicin and 5-fluorouracil; increased migration and invasion, increased amount of integrin-linked kinase (ILK) and decreased amounts of non-receptor tyrosine kinase (Src) and pSrc(Y418). Knockdown of ILK and integrin ß5 in cells expressing integrin αvß3 ruled out their involvement in drug resistance. Opposite, Src knockdown in Cal27 cells which led to a reduction in pSrc(Y418), as well as treatment with the pSrc(Y418) inhibitors dasatinib and PP2, conferred resistance to all four anticancer drugs, indicating that the loss of pSrc(Y418) is responsible for the observed effect. We identified differential integrin signaling between Cal27 and integrin αvß3-expressing cells. In Cal27 cells integrin αv heterodimers signal through pSrc(Y418) while this is not the case in integrin αvß3-expressing cells. Finally, we show that dasatinib counteracts the effect of cisplatin in two additional head and neck squamous cell carcinoma (HNSCC) cell lines Cal33 and Detroit562. Our results suggest that pSrc(Y418) inhibitors, potential drugs for cancer therapy, may reduce therapeutic efficacy if combined with chemotherapeutics, and might not be recommended for HNSCC treatment.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/patologia
Resistência a Medicamentos Antineoplásicos/fisiologia
Integrina alfaVbeta3/fisiologia
Proteínas de Neoplasias/fisiologia
Proteínas Proto-Oncogênicas pp60(c-src)/fisiologia
Neoplasias da Língua/patologia
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/metabolismo
Linhagem Celular Tumoral
Movimento Celular
Cisplatino/farmacologia
Dasatinibe/farmacologia
Doxorrubicina/farmacologia
Sinergismo Farmacológico
Fluoruracila/farmacologia
Regulação Neoplásica da Expressão Gênica
Genes src
Seres Humanos
Integrina alfaVbeta3/biossíntese
Integrina alfaVbeta3/genética
Cadeias beta de Integrinas/fisiologia
Mitomicina/farmacologia
Invasividade Neoplásica
Proteínas de Neoplasias/biossíntese
Proteínas de Neoplasias/genética
Mutação Puntual
Multimerização Proteica
Proteínas Serina-Treonina Quinases/fisiologia
Proteínas Proto-Oncogênicas pp60(c-src)/genética
Interferência de RNA
Neoplasias da Língua/genética
Neoplasias da Língua/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (ITGB5 protein, human); 0 (Integrin alphaVbeta3); 0 (Integrin beta Chains); 0 (Neoplasm Proteins); 50SG953SK6 (Mitomycin); 80168379AG (Doxorubicin); EC 2.7.1.- (integrin-linked kinase); EC 2.7.10.2 (Proto-Oncogene Proteins pp60(c-src)); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); Q20Q21Q62J (Cisplatin); RBZ1571X5H (Dasatinib); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160425
[St] Status:MEDLINE


  8 / 928 MEDLINE  
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[PMID]:27100152
[Au] Autor:Dong X; Ju S; Chen J; Meng F; Sun P; Li Y; Wang X; Wang Y; Liu J; Chang S; Zhao P; Cui Z
[Ad] Endereço:a College of Veterinary Medicine, Shandong Agricultural University , Taian , People's Republic of China.
[Ti] Título:Karyotype analysis of the acute fibrosarcoma from chickens infected with subgroup J avian leukosis virus associated with v-src oncogene.
[So] Source:Avian Pathol;45(2):202-7, 2016.
[Is] ISSN:1465-3338
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To understand the cytogenetic characteristics of acute fibrosarcoma in chickens infected with the subgroup J avian leukosis virus associated with the v-src oncogene, we performed a karyotype analysis of fibrosarcoma cell cultures. Twenty-nine of 50 qualified cell culture spreads demonstrated polyploidy of some macrochromosomes, 21 of which were trisomic for chromosome 7, and others were trisomic for chromosomes 3, 4, 5 (sex chromosome w), and 10. In addition, one of them was trisomic for both chromosome 7 and the sex chromosome 5 (w). In contrast, no aneuploidy was found for 10 macrochromosomes of 12 spreads of normal chicken embryo fibroblast cells, although aneuploidy for some microchromosomes was demonstrated in five of the 12 spreads. The cytogenetic mosaicism or polymorphism of the aneuploidy in the acute fibrosarcoma described in this study suggests that the analysed cells are polyclonal.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/genética
Leucose Aviária/virologia
Galinhas/virologia
Aberrações Cromossômicas
Fibrossarcoma/veterinária
Genes src/genética
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Leucose Aviária/genética
Vírus da Leucose Aviária/isolamento & purificação
Embrião de Galinha
Feminino
Fibrossarcoma/genética
Fibrossarcoma/virologia
Cariótipo
Cariotipagem/veterinária
Polimorfismo Genético
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170406
[Lr] Data última revisão:
170406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160422
[St] Status:MEDLINE
[do] DOI:10.1080/03079457.2016.1142501


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[PMID]:26842006
[Au] Autor:Wang Y; Li J; Li Y; Fang L; Sun X; Chang S; Zhao P; Cui Z
[Ad] Endereço:College of Animal Science and Veterinary Medicine, Shandong Agricultural University,Daizong Road No. 61, Tai'an, Shandong, 271018, PRChina.
[Ti] Título:Identification of avian leukosis virus subgroup J-associated acutely transforming viruses carrying the v-src oncogene in layer chickens.
[So] Source:J Gen Virol;97(5):1240-8, 2016 05.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To elucidate the molecular basis for the rapid oncogenicity of an acutely transforming avian leukosis virus (ALV), isolated from fibrosarcomas in Hy-Line Brown commercial layer chickens infected with ALV subgroup J (ALV-J), the complete genomic structure of the provirus was determined. In addition to ALV-J replication-complete virus SDAU1102, five proviral DNA genomes, named SJ-1, SJ-2, SJ-3, SJ-4 and SJ-5, carrying different lengths of the v-src oncogene were amplified from original tumours and chicken embryo fibroblasts (CEFs) infected with viral stocks. The genomic sequences of the SJ-1-SJ-5 provirus were closely related to that of SDAU1102 but were defective. The results of Western blot analysis and immunohistochemical staining also showed overexpression of the p60v-src protein in infected CEFs and tumour tissue. To the best of our knowledge, this is the first report of the isolation and identification of acutely transforming viruses carrying the v-src oncogene with ALV-J as the helper virus. It also offers insight into the generation of acutely transforming ALVs carrying the v-src oncogene.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/classificação
Vírus da Leucose Aviária/genética
Leucose Aviária/virologia
Galinhas
Genes src
Genoma Viral
[Mh] Termos MeSH secundário: Animais
Leucose Aviária/diagnóstico
Sequência de Bases
DNA Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Viral)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171127
[Lr] Data última revisão:
171127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160205
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000420


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[PMID]:26720617
[Au] Autor:Lai CY; Lin TB; Hsieh MC; Chen GD; Peng HY
[Ad] Endereço:From the *Department of Medicine, Mackay Medical College, New Taipei, Taiwan; †Department of Veterinary Medicine, College of Veterinary Medicine, National Chung-Hsing University, Taichung, Taiwan; ‡Department of Biotechnology, Asia University, Taichung, Taiwan; §Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; ‖Department of Physiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; ¶Department of Physiology, School of Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan; and #Department of Obstetrics and Gynecology, Chung-Shan Medical University Hospital, Chung-Shan Medical University, Taichung, Taiwan.
[Ti] Título:SIRPα1-SHP2 Interaction Regulates Complete Freund Adjuvant-Induced Inflammatory Pain via Src-Dependent GluN2B Phosphorylation in Rats.
[So] Source:Anesth Analg;122(3):871-81, 2016 Mar.
[Is] ISSN:1526-7598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The elusiveness of pain mechanisms is a major impediment in developing effective clinical treatments. We examined whether the signal regulatory protein α1 (SIRPα1)-activated spinal Src homology-2 domain-containing protein tyrosine phosphatase 2 (SHP2)/Src cascade and the downstream GluN2B phosphorylation play a role in inflammatory pain. METHODS: At hour 3 and days 1, 3, 5, and 10 after the intraplantar injection of complete Freund adjuvant (CFA), we assessed paw withdrawal latency using the Hargreaves test and analyzed dorsal horn samples (L4-L5) by Western blotting and immunoprecipitation. RESULTS: Intraplantar CFA injection provoked the behavioral hyperalgesia in the ipsilateral hind-paw along with SIRPα1, phosphorylated SHP2 (pSHP2), phosphorylated Src (pSrc), and phosphorylated GluN2B expressions and total SHP2 (tSHP2)-SIRPα1/pSHP2/pSrc and total Src (tSrc)-SIRPα1/pSHP2/pSrc coprecipitation in the ipsilateral dorsal horn. Although both of them failed to show an effect on CFA-enhanced SIRPα1 expression, spinal administration with SIRPα1-neutralizing antibody (10, 50, and 100 µg, 10 µL) and 8-Hydroxy-7-[(6-sulfo-2-naphthyl)azo]-5-quinolinesulfonic acid (NSC 8787; an SHP2 antagonist, 1, 10, and 100 µM, 10 µL) dose-dependently attenuated the behavioral hyperalgesia, SHP2 and Src phosphorylation, and tSHP2-SIRPα1/pSHP2/pSrc coprecipitation at day 1 after CFA injection. Intrathecal application of 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2; a Src-family kinase inhibitor, 10, 30, and 50 nM, 10 µL) exhibited a similar effect as these agents, except that it failed to ameliorate CFA-enhanced SHP2 phosphorylation and tSHP2-SIRPα1/pSHP2 coprecipitation. CONCLUSIONS: CFA-induced spinal SIRPα1 expression, which triggers SHP2, and Src phosphorylation, which subsequently induced pSrc-GluN2B interaction to mediate the GluN2B activation, contribute to spinal plasticity underlying the maintenance of inflammatory pain. These findings provide a possible strategy for pain relief by targeting to spinal SIRPα1-SHP2 coupling.
[Mh] Termos MeSH primário: Genes src/genética
Inflamação/fisiopatologia
Dor/fisiopatologia
Proteína Tirosina Fosfatase não Receptora Tipo 11/antagonistas & inibidores
Receptores Imunológicos/antagonistas & inibidores
Receptores de N-Metil-D-Aspartato/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/farmacologia
Comportamento Animal/efeitos dos fármacos
Inibidores Enzimáticos/farmacologia
Adjuvante de Freund
Hiperalgesia/genética
Hiperalgesia/metabolismo
Hiperalgesia/psicologia
Inflamação/induzido quimicamente
Injeções Espinhais
Masculino
Dor/induzido quimicamente
Fosforilação
Proteína Tirosina Fosfatase não Receptora Tipo 11/genética
Ratos
Ratos Sprague-Dawley
Receptores Imunológicos/genética
Receptores de N-Metil-D-Aspartato/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Enzyme Inhibitors); 0 (NR2B NMDA receptor); 0 (Receptors, Immunologic); 0 (Receptors, N-Methyl-D-Aspartate); 0 (SIRPalpha protein, rat); 9007-81-2 (Freund's Adjuvant); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11); EC 3.1.3.48 (Ptpn11 protein, rat)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160219
[Lr] Data última revisão:
160219
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160101
[St] Status:MEDLINE
[do] DOI:10.1213/ANE.0000000000001116



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