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[PMID]:27779422
[Au] Autor:Kouzaki H; Matsumoto K; Kikuoka H; Kato T; Tojima I; Shimizu S; Kita H; Shimizu T
[Ad] Endereço:1 Department of Otorhinolaryngology, Shiga University of Medical Science, Otsu, Shiga, Japan; and.
[Ti] Título:Endogenous Protease Inhibitors in Airway Epithelial Cells Contribute to Eosinophilic Chronic Rhinosinusitis.
[So] Source:Am J Respir Crit Care Med;195(6):737-747, 2017 Mar 15.
[Is] ISSN:1535-4970
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Cystatin A and SPINK5 are endogenous protease inhibitors (EPIs) that may play key roles in epithelial barrier function. OBJECTIVES: To investigate the roles of EPIs in the pathogenesis of chronic rhinosinusitis (CRS). METHODS: We examined the expression of cystatin A and SPINK5 in the nasal epithelial cells of patients with CRS. Additionally, the in vitro effects of recombinant EPIs on the secretion of the epithelial-derived cytokines IL-25, IL-33, and thymic stromal lymphopoietin in airway epithelial cells, and the in vivo effects of recombinant EPIs in the nasal epithelium of mice exposed to multiple airborne allergens (MAA) were examined. MEASUREMENTS AND MAIN RESULTS: Compared with control subjects and patients with noneosinophilic CRS, patients with eosinophilic CRS showed significantly lower protein and mRNA expression of cystatin A and SPINK5 in the nasal epithelium. Allergen-induced production of IL-25, IL-33, and thymic stromal lymphopoietin in normal human bronchial epithelial cells was inhibited by treatment with recombinant cystatin A or SPINK5. Conversely, the production of these cytokines was increased when cystatin A or SPINK5 were knocked down with small interfering RNA. Chronic MAA exposure induced goblet cell metaplasia and epithelial disruption in mouse nasal epithelium and decreased the tissue expression and nasal lavage levels of cystatin A and SPINK5. Intranasal instillations of recombinant EPIs attenuated this MAA-induced pathology. CONCLUSIONS: Cystatin A and SPINK5 play an important role in protecting the airway epithelium from exogenous proteases. The preservation of EPIs may have a therapeutic benefit in intractable airway inflammation, such as eosinophilic CRS.
[Mh] Termos MeSH primário: Eosinofilia/metabolismo
Células Epiteliais/metabolismo
Inibidores de Proteases/metabolismo
Rinite/metabolismo
Sinusite/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Doença Crônica
Cistatina A/metabolismo
Eosinofilia/complicações
Feminino
Seres Humanos
Interleucina-17/metabolismo
Interleucina-33/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Meia-Idade
Mucosa Nasal/metabolismo
Proteínas Secretadas Inibidoras de Proteinases/metabolismo
Rinite/complicações
Inibidor de Serinopeptidase do Tipo Kazal 5
Sinusite/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cystatin A); 0 (Interleukin-17); 0 (Interleukin-33); 0 (Protease Inhibitors); 0 (Proteinase Inhibitory Proteins, Secretory); 0 (SPINK5 protein, human); 0 (Serine Peptidase Inhibitor Kazal-Type 5)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1164/rccm.201603-0529OC


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[PMID]:28163207
[Au] Autor:Schröder H; Fischer R; Sollfrank L; Paulsen F; Bräuer L; Schicht M
[Ad] Endereço:Department of Anatomy II, Friedrich Alexander University Erlangen-Nürnberg (FAU), Erlangen, Germany. Electronic address: henrik.schroeder@fau.de.
[Ti] Título:Expression of recombinant surfactant protein SFTA3 in the human kidney cell line HEK 293T.
[So] Source:Ann Anat;211:149-157, 2017 May.
[Is] ISSN:1618-0402
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Pulmonary surfactant is broadly known to keep the lung dry, clean and open by lowering the surface tension of the fluid-film that lines the alveoli. The surfactant's protein component, the so called surfactant proteins (SPs), make up a multifunctional protein family. In addition to the four "classical" surfactant proteins (SP-A, SP-B, SP-C and SP-D), which possess immunologic as well as surfactant regulatory properties, two novel putative surfactant proteins (SFTA2 and SFTA3) have recently been described. Neither of them shows sequential nor structural similarity with the already known surfactant proteins. However, bioinformatic analyses as well as first molecular-biological studies reveal properties that have already been described for known surfactant proteins. In our present work we introduce a technique to synthesize, purify and stabilize recombinant SFTA3 derived from the human embryonic kidney cell line HEK 293T. This will provide investigators with a valuable source of further examination and characterization of this fascinating novel member of the surfactant protein family.
[Mh] Termos MeSH primário: Cistatina A/genética
Cistatina A/metabolismo
Células HEK293/fisiologia
Engenharia de Proteínas/métodos
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/genética
[Mh] Termos MeSH secundário: Clonagem Molecular/métodos
Cistatina A/química
Seres Humanos
Proteínas Recombinantes/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cystatin A); 0 (Recombinant Proteins); 0 (Stfa3 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE


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[PMID]:27825931
[Au] Autor:Morris CA; El-Hiti GA; Weeks I; Woodhead S; Smith K; Kille P
[Ad] Endereço:School of Biosciences, Cardiff University, Cardiff CF10 3AT, UK; School of Medicine, Cardiff University, Tenovus Building, Heath Park, Cardiff CF14 4XN, UK. Electronic address: morrisc10@cardiff.ac.uk.
[Ti] Título:Quantitative analysis of gene expression changes in response to genotoxic compounds.
[So] Source:Toxicol In Vitro;39:15-28, 2017 Mar.
[Is] ISSN:1879-3177
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Techniques that quantify molecular endpoints sufficiently sensitive to identify and classify potentially toxic compounds have wide potential for high-throughput in vitro screening. Expression of three genes, RAD51C, TP53 and cystatin A (CSTA), in HEPG2 cells was measured by Q-PCR amplification. In parallel, we developed alternative assays for the same 3 gene signature based on an acridinium-ester chemiluminescent reporter molecule. HEPG2 cells were challenged with eighteen different compounds (n=18) chosen to represent compounds that are genotoxic (n=8), non-genotoxic non-carcinogenic (n=2) or have a less well defined mechanism of action with respect to genotoxicity (n=8). At least one of the three genes displayed dysregulated expression in the majority of compounds tested by Q-PCR and ten compounds changed the CSTA expression significantly. Acridinium-ester labelled probes for the three genes were synthesised and tested. Analytical sensitivity was characterised and suggested a limit of detection generally better than 0.1fmol but often 10-50 attomol. A linear amplification step was optimised and this quantitative method detected statistically significant increases in RAD51C and CSTA expression in agreement with the Q-PCR results, demonstrating the potential of this technology. The broad agreement of the amplified chemiluminescent method and Q-PCR in measuring gene expression suggests wider potential application for this chemiluminescent technology.
[Mh] Termos MeSH primário: Cistatina A/genética
Proteínas de Ligação a DNA/genética
Expressão Gênica/efeitos dos fármacos
Mutagênicos/toxicidade
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Células Hep G2
Seres Humanos
Medições Luminescentes
Reação em Cadeia da Polimerase/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cystatin A); 0 (DNA-Binding Proteins); 0 (Mutagens); 0 (RAD51C protein, human); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 80209-89-8 (CSTA protein, human)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170327
[Lr] Data última revisão:
170327
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161110
[St] Status:MEDLINE


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[PMID]:27666198
[Au] Autor:Zhang J; Zhang G; Ni C; Cheng R; Liang J; Li M; Yao Z
[Ad] Endereço:Department of Dermatology, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai 200092, P.R. China.
[Ti] Título:Nagashima-type palmoplantar keratosis in a Chinese Han population.
[So] Source:Mol Med Rep;14(5):4049-4054, 2016 Nov.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Nagashima-type palmoplantar keratosis (NPPK) is an autosomal recessive form of palmoplantar keratoderma (PPK), which is caused by mutations in the SERPINB7 gene. NPPK has only been reported in Japanese and Chinese populations. The present study was conducted on 12 unrelated Chinese patients who were clinically predicted to suffer from NPPK. Mutation screening was performed by direct sequencing of the entire coding regions of SERPINB7, SLURP1, AQP5, CSTA, KRT1 and KRT9 genes. Direct sequencing of SERPINB7 revealed five homozygous founder mutations (c.796C>T) and four compound heterozygous mutations in nine patients, including one novel mutation (c.122_127delTGGTCC). Nine out of the 12 patients were diagnosed with NPPK due to SERPINB7 pathogenic mutations, and the results expanded the known mutation spectrum of NPPK. Taking the other seven reported Chinese patients, who had been definitively diagnosed with NPPK by genetic testing, into account, the present study further demonstrated that NPPK is a common entity in Mainland China, and c.796C>T is the most prevalent mutation and exerts a founder effect. Furthermore, the NPPK cases described in the current study presented a consistently mild phenotype, as compared with the degrees of phenotypic variability associated with other types of relatively severe PPK, including Mal de Meleda and Olmsted syndrome.
[Mh] Termos MeSH primário: Testes Genéticos
Ceratodermia Palmar e Plantar/genética
Serpinas/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Antígenos Ly/genética
Aquaporina 5/genética
Grupo com Ancestrais do Continente Asiático
Criança
Pré-Escolar
China
Cistatina A/genética
Feminino
Efeito Fundador
Heterozigoto
Sequenciamento de Nucleotídeos em Larga Escala
Homozigoto
Seres Humanos
Lactente
Queratina-1/genética
Queratina-9/genética
Ceratodermia Palmar e Plantar/patologia
Masculino
Meia-Idade
Mutação
Linhagem
Ativador de Plasminogênio Tipo Uroquinase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AQP5 protein, human); 0 (Antigens, Ly); 0 (Aquaporin 5); 0 (Cystatin A); 0 (KRT1 protein, human); 0 (KRT9 protein, human); 0 (Keratin-1); 0 (Keratin-9); 0 (SERPINB7 protein, human); 0 (SLURP1 protein, human); 0 (Serpins); 80209-89-8 (CSTA protein, human); EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170410
[Lr] Data última revisão:
170410
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160927
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2016.5757


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[PMID]:26967115
[Au] Autor:Maruyama R; Shimizu M; Ishijima T; Nakai Y; Inoue J; Sato R
[Ad] Endereço:a Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences , The University of Tokyo , Tokyo , Japan.
[Ti] Título:Searching for novel ATF4 target genes in human hepatoma cells by microarray analysis.
[So] Source:Biosci Biotechnol Biochem;80(6):1149-54, 2016 Jun.
[Is] ISSN:1347-6947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Activating transcription factor 4 (ATF4) is a transcription factor with an important biological activity. ATF4 is induced by various stresses, such as endoplasmic reticulum stress, through the phosphorylation of eukaryotic translation initiation factor 2α. ATF4 is also involved in lipid metabolism. In the present study, we performed a microarray experiment to identify new ATF4 target genes, particularly those involved in lipid metabolism, and identified C12orf39, CSTA, and CALCB as novel ATF4 target genes. An amino acid response element (AARE) as an ATF4-binding site is present in the promoter regions of these genes. In a detailed analysis using luciferase assay, we showed that ATF4 activated C12orf39 promoter activity and that this activation was diminished by deletion or mutation of the AARE sequence in the promoter region. Our results suggest that C12orf39, CSTA, and CALCB are novel ATF4 target genes and that C12orf39 promoter activity is activated by ATF4 through AARE.
[Mh] Termos MeSH primário: Fator 4 Ativador da Transcrição/genética
Peptídeo Relacionado com Gene de Calcitonina/genética
Cistatina A/genética
Regulação Neoplásica da Expressão Gênica
Hepatócitos/metabolismo
Hormônios Peptídicos/genética
[Mh] Termos MeSH secundário: Fator 4 Ativador da Transcrição/metabolismo
Sítios de Ligação
Peptídeo Relacionado com Gene de Calcitonina/metabolismo
Linhagem Celular Tumoral
Cistatina A/metabolismo
Fator de Iniciação 2 em Eucariotos/genética
Fator de Iniciação 2 em Eucariotos/metabolismo
Perfilação da Expressão Gênica
Genes Reporter
Hepatócitos/patologia
Seres Humanos
Metabolismo dos Lipídeos/genética
Luciferases/genética
Luciferases/metabolismo
Análise em Microsséries
Mutação
Hormônios Peptídicos/metabolismo
Ligação Proteica
Elementos de Resposta
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATF4 protein, human); 0 (C12ORF39 protein, human); 0 (Cystatin A); 0 (Eukaryotic Initiation Factor-2); 0 (Peptide Hormones); 145891-90-3 (Activating Transcription Factor 4); 80209-89-8 (CSTA protein, human); 83652-28-2 (Calcitonin Gene-Related Peptide); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170117
[Lr] Data última revisão:
170117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160312
[St] Status:MEDLINE
[do] DOI:10.1080/09168451.2016.1146072


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[PMID]:26753874
[Au] Autor:Lin YY; Chen ZW; Lin ZP; Lin LB; Yang XM; Xu LY; Xie Q
[Ad] Endereço:Department of Human Anatomy, Histology and Embryology, School of Basic Medical Science, Putian University, Putian, Fujian, China.
[Ti] Título:Tissue Levels of Stefin A and Stefin B in Hepatocellular Carcinoma.
[So] Source:Anat Rec (Hoboken);299(4):428-38, 2016 Apr.
[Is] ISSN:1932-8494
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stefins have been reported to be associated with the progression and metastasis of various malignant tumors. However, the expressions of stefins in hepatocellular carcinoma (HCC) have not been well-defined. In this study, the protein levels of stefin A and stefin B were assessed by immunohistochemical staining, and the mRNA levels were quantified by real-time polymerase chain reaction in 85 primary HCC tissues, 85 surrounding non-cancerous tissues, and 9 normal hepatic tissues. The immunohistochemical staining of cathepsin B and cathepsin D, and the ratio of cathepsins to stefins were assessed. The mRNA expressions of stefin A and stefin B in HCC tissues were significantly higher than surrounding noncancerous tissues and normal hepatic tissues, respectively. A significant positive relationship of stefin A and stefin B was found with node metastasis, tumor size, and Edmondson grade for HCC. Univariate and multivariate analyses revealed that Edmondson grade and stefin B expression were independent factors associated with the risk of lymph node metastasis in HCC. The ratios of cathepsin B to stefin A, cathepsin D to stefin A, cathepsin B to stefin B and cathepsin D to stefin B of the HCC group were significantly higher than that of the surrounding noncancerous group. A significant positive correlation between the ratio of cathepsins to stefins (cathepsin B/stefin A, cathepsin B/stefin B and cathepsin D/stefin B) and node metastasis was demonstrated. We concluded that high expressions of stefin A and stefin B may be an important factor contributing to the development and metastasis of HCC.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Carcinoma Hepatocelular/metabolismo
Catepsinas/metabolismo
Cistatina A/metabolismo
Cistatina B/metabolismo
Neoplasias Hepáticas/metabolismo
Fígado/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores Tumorais/genética
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/secundário
Estudos de Casos e Controles
Catepsinas/genética
Cistatina A/genética
Cistatina B/genética
Feminino
Seguimentos
Seres Humanos
Técnicas Imunoenzimáticas
Fígado/patologia
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Metástase Linfática
Masculino
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Prognóstico
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CSTB protein, human); 0 (Cystatin A); 80209-89-8 (CSTA protein, human); 88844-95-5 (Cystatin B); EC 3.4.- (Cathepsins)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160113
[St] Status:MEDLINE
[do] DOI:10.1002/ar.23311


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[PMID]:26684698
[Au] Autor:Muttardi K; Nitoiu D; Kelsell DP; O'Toole EA; Batta K
[Ad] Endereço:Department of Dermatology, Watford General Hospital, Watford, Hertfordshire, UK.
[Ti] Título:Acral peeling skin syndrome associated with a novel CSTA gene mutation.
[So] Source:Clin Exp Dermatol;41(4):394-8, 2016 Jun.
[Is] ISSN:1365-2230
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Acral peeling skin syndrome (APSS) is a rare autosomal recessive condition, characterized by asymptomatic peeling of the skin of the hands and feet, often linked to mutations in the gene TGM5. However, more recently recessive loss of function mutations in CSTA, encoding cystatin A, have been linked with APSS and exfoliative ichthyosis. We describe the clinical features in two sisters with APSS, associated with a novel large homozygous deletion encompassing exon 1 of CSTA.
[Mh] Termos MeSH primário: Cistatina A/genética
Cistatina A/metabolismo
Mutação/genética
Dermatopatias/congênito
Pele/patologia
Pele/fisiopatologia
[Mh] Termos MeSH secundário: Criança
Pré-Escolar
Cistatina A/fisiologia
Análise Mutacional de DNA
Eritema/patologia
Grupo com Ancestrais do Continente Europeu
Feminino
/patologia
Mãos/patologia
Homozigoto
Seres Humanos
Hiperopia/congênito
Ictiose/etiologia
Ictiose/genética
Linhagem
Dermatopatias/genética
Dermatopatias/patologia
Dermatopatias/fisiopatologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cystatin A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151220
[St] Status:MEDLINE
[do] DOI:10.1111/ced.12777


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[PMID]:26481272
[Au] Autor:Chauhan S; Tomar RS
[Ad] Endereço:Laboratory of Chromatin Biology, Department of Biological Sciences, Indian Institute of Science Education and Research, Bhopal, 462023, India.
[Ti] Título:Efficient expression and purification of biologically active human cystatin proteins.
[So] Source:Protein Expr Purif;118:10-7, 2016 Feb.
[Is] ISSN:1096-0279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cystatins are reversible cysteine protease inhibitor proteins. They are known to play important roles in controlling cathepsins, neurodegenerative disease, and in immune system regulation. Production of recombinant cystatin proteins is important for biochemical and function characterization. In this study, we cloned and expressed human stefin A, stefin B and cystatin C in Escherichia coli. Human stefin A, stefin B and cystatin C were purified from soluble fraction. For cystatin C, we used various chaperone plasmids to make cystatin C soluble, as it is reported to localize in inclusion bodies. Trigger factor, GroES-GroEL, DnaK-DnaJ-GrpE chaperones lead to the presence of cystatin C in the soluble fraction. Immobilized metal affinity chromatography, glutathione sepharose and anion exchange chromatography techniques were employed for efficient purification of these proteins. Their biological activities were tested by inhibition assays against cathepsin L and H3 protease.
[Mh] Termos MeSH primário: Cistatina A/genética
Cistatina A/isolamento & purificação
Cistatina B/genética
Cistatina B/isolamento & purificação
Cistatina C/genética
Cistatina C/isolamento & purificação
[Mh] Termos MeSH secundário: Catepsina L/antagonistas & inibidores
Catepsina L/química
Cistatina A/química
Cistatina A/metabolismo
Cistatina B/química
Cistatina B/metabolismo
Cistatina C/química
Cistatina C/metabolismo
Endopeptidases/química
Inibidores Enzimáticos/química
Inibidores Enzimáticos/isolamento & purificação
Inibidores Enzimáticos/metabolismo
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Seres Humanos
Cinética
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/isolamento & purificação
Proteínas Recombinantes/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cystatin A); 0 (Cystatin C); 0 (Enzyme Inhibitors); 0 (Recombinant Proteins); 88844-95-5 (Cystatin B); EC 3.4.- (Endopeptidases); EC 3.4.22.15 (Cathepsin L); EC 3.4.99.- (histone proteases)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151021
[St] Status:MEDLINE


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[PMID]:26634210
[Au] Autor:Tang M; Ou N; Li C; Lu A; Li J; Ma L; Zhong W; Gao J; Zheng Y; Cai Y
[Ad] Endereço:Wuzhou Health System Key Laboratory for Nasopharyngeal Carcinoma Etiology and Molecular Mechanism, Wuzhou, Guangxi 543002, China ; Department of Clinical Laboratory, Wuzhou Red Cross Hospital, Wuzhou, Guangxi 543002, China.
[Ti] Título:Expression and Prognostic Significance of Macrophage Inflammatory Protein-3 Alpha and Cystatin A in Nasopharyngeal Carcinoma.
[So] Source:Biomed Res Int;2015:617143, 2015.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aims to investigate the expression of macrophage inflammatory protein-3 alpha (MIP-3α) and cystatin A in nasopharyngeal carcinoma (NPC) and their association with clinical characteristics and prognosis. Primary tumor specimens from 114 NPC patients and associated clinical follow-up data were collected, and the expression of MIP-3α and cystatin A proteins was investigated by immunohistochemistry. Expression of MIP-3α was significantly associated with TNM stage in patients with NPC (P < 0.05). NPC patients with positive expression of MIP-3α exhibited shorter median overall survival (OS) and distant metastasis-free survival (DMFS), compared with patients with negative expression (OS: 50.5 months versus 59.0 months, P = 0.013; DMFS: 50.1 months versus 60.2 months, P = 0.003). NPC patients with positive expression of cystatin A exhibited shorter median OS, local recurrence-free survival (LRFS), and DMFS, compared with patients with negative expression (OS: 51.1 months versus 60.0 months, P = 0.004; LRFS: 54.5 months versus 59.5 months, P = 0.036; DMFS: 52.3 months versus 58.8 months, P = 0.036). Both MIP-3α and cystatin A overexpressions in NPC tumor tissues were strong independent factors of poor prognosis in NPC patients. MIP-3α and cystatin A expressions may be valuable prognostic markers in NPC patients.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Quimiocina CCL20/metabolismo
Cistatina A/metabolismo
Neoplasias Nasofaríngeas/metabolismo
Neoplasias Nasofaríngeas/mortalidade
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinoma
China/epidemiologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Neoplasias Nasofaríngeas/radioterapia
Prevalência
Prognóstico
Reprodutibilidade dos Testes
Medição de Risco/métodos
Sensibilidade e Especificidade
Taxa de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CCL20 protein, human); 0 (Chemokine CCL20); 0 (Cystatin A); 80209-89-8 (CSTA protein, human)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151204
[St] Status:MEDLINE
[do] DOI:10.1155/2015/617143


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[PMID]:25785582
[Au] Autor:Gupta A; Nitoiu D; Brennan-Crispi D; Addya S; Riobo NA; Kelsell DP; Mahoney MG
[Ad] Endereço:Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia, Pennsylvania, United States of America.
[Ti] Título:Cell cycle- and cancer-associated gene networks activated by Dsg2: evidence of cystatin A deregulation and a potential role in cell-cell adhesion.
[So] Source:PLoS One;10(3):e0120091, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell-cell adhesion is paramount in providing and maintaining multicellular structure and signal transmission between cells. In the skin, disruption to desmosomal regulated intercellular connectivity may lead to disorders of keratinization and hyperproliferative disease including cancer. Recently we showed transgenic mice overexpressing desmoglein 2 (Dsg2) in the epidermis develop hyperplasia. Following microarray and gene network analysis, we demonstrate that Dsg2 caused a profound change in the transcriptome of keratinocytes in vivo and altered a number of genes important in epithelial dysplasia including: calcium-binding proteins (S100A8 and S100A9), members of the cyclin protein family, and the cysteine protease inhibitor cystatin A (CSTA). CSTA is deregulated in several skin cancers, including squamous cell carcinomas (SCC) and loss of function mutations lead to recessive skin fragility disorders. The microarray results were confirmed by qPCR, immunoblotting, and immunohistochemistry. CSTA was detected at high level throughout the newborn mouse epidermis but dramatically decreased with development and was detected predominantly in the differentiated layers. In human keratinocytes, knockdown of Dsg2 by siRNA or shRNA reduced CSTA expression. Furthermore, siRNA knockdown of CSTA resulted in cytoplasmic localization of Dsg2, perturbed cytokeratin 14 staining and reduced levels of desmoplakin in response to mechanical stretching. Both knockdown of either Dsg2 or CSTA induced loss of cell adhesion in a dispase-based assay and the effect was synergistic. Our findings here offer a novel pathway of CSTA regulation involving Dsg2 and a potential crosstalk between Dsg2 and CSTA that modulates cell adhesion. These results further support the recent human genetic findings that loss of function mutations in the CSTA gene result in skin fragility due to impaired cell-cell adhesion: autosomal-recessive exfoliative ichthyosis or acral peeling skin syndrome.
[Mh] Termos MeSH primário: Ciclo Celular
Cistatina A/metabolismo
Desmogleína 2/metabolismo
Redes Reguladoras de Genes
[Mh] Termos MeSH secundário: Animais
Adesão Celular
Linhagem Celular Tumoral
Cistatina A/genética
Desmogleína 2/genética
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Queratinócitos/citologia
Queratinócitos/metabolismo
Camundongos
Camundongos Transgênicos
Análise de Sequência com Séries de Oligonucleotídeos
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Cystatin A); 0 (Desmoglein 2)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150319
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0120091



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