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  1 / 101 MEDLINE  
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[PMID]:27878264
[Au] Autor:Zhou T; Li Y; Yang L; Liu L; Ju Y; Li C
[Ad] Endereço:Breast Disease Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China.
[Ti] Título:Silencing of ANXA3 expression by RNA interference inhibits the proliferation and invasion of breast cancer cells.
[So] Source:Oncol Rep;37(1):388-398, 2017 Jan.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:The present study aimed to explore the expression of Annexin A3 (ANXA3) in breast cancer cells and the mechanisms involved in the regulatory effects of ANXA3 on proliferation, invasion and migration of breast cancer cells. Fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting were used to measure the expression of ANXA3 mRNA and protein in two breast cancer cell lines (MDA-MB-231 and MCF-7). Three ANXA3 silencing shRNA plasmids (ANXA3-sh1-3) and one negative control plasmid were constructed, and the Lipofectamine transfection method was used for transfecting human breast cancer cell line MDA-MB-231. Flow cytometry was used to measure the transfection efficiency. The expression of ANXA3 protein was measured by western blotting. Cell cycle distribution and apoptosis were assessed by flow cytometry. Migration and invasion of the transfected cells were evaluated using wound healing and Transwell assays, respectively. The expression levels of ANXA3 mRNA and protein were significantly higher in the MDA-MB-231 cells than levels in the MCF-7 cells. Western blotting showed that the ANXA3 protein level was significantly lower in the MDA-MB-231-Sh cells than that in the MDA-MB-231 and MDA-MB-231-NC cells. In addition, the percentage of G0/1 cells and the apoptosis rate were significantly higher, while the cell proliferation rate was significantly lower, in the MDA-MB-231-Sh cells when compared with the MDA-MB-231-NC and MDA-MB-231 cells. The cell migration and invasion abilities were also lower in the MDA-MB-231-Sh cells than these abilities in the MDA-MB-231-NC and MDA-MB-231 cells. The present study investigated the relationships between ANXA3 and proliferation, apoptosis, migration and invasion of breast cancer cells to elucidate the mechanisms involved in the development, progression, invasion and metastasis of breast cancer.
[Mh] Termos MeSH primário: Anexina A3/genética
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
[Mh] Termos MeSH secundário: Anexina A3/metabolismo
Apoptose/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Feminino
Citometria de Fluxo/métodos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Inativação Gênica
Vetores Genéticos
Seres Humanos
Lentivirus/genética
Células MCF-7
Puromicina
Interferência de RNA
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANXA3 protein, human); 4A6ZS6Q2CL (Puromycin); EC 3.1.4.43 (Annexin A3)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170322
[Lr] Data última revisão:
170322
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE
[do] DOI:10.3892/or.2016.5251


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[PMID]:27995049
[Au] Autor:Liu YF; Liu QQ; Zhang YH; Qiu JH
[Ad] Endereço:Department of Basic Medical Sciences, Medical College, Xiamen University, Xiamen, Fujian, China.
[Ti] Título:Annexin A3 Knockdown Suppresses Lung Adenocarcinoma.
[So] Source:Anal Cell Pathol (Amst);2016:4131403, 2016.
[Is] ISSN:2210-7185
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Our previous study identified an elevated abundance of annexin A3 (Anxa3) as a novel prognostic biomarker of lung adenocarcinoma (LADC) through quantitative proteomics analysis. However, the biological functions of Anxa3 in LADC are not fully clear. In this study, and assays were performed to investigate the effects of Anxa3 downregulation on the growth, migration, invasion, metastasis, and signaling pathway activation of LADC cells. After Anxa3 downregulation, the growth of A549 and LTEP-a2 LADC cells was slowed and they showed decreased migration and invasion . Anxa3 knockdown significantly inhibited tumor formation by A549 cells ; while many metastases were formed by control A549 cells, there were obvious reductions in the numbers of lung, liver, and brain metastases formed by Anxa3 knockdown in A549 cells. Furthermore, Anxa3 knockdown significantly decreased MMP-2 and N-cadherin expression and increased E-cadherin expression both in cell lines and in tumor nodules examined during tumorigenesis assays. Interestingly, Anxa3 downregulation reduced the phosphorylated levels of MEK and ERK. In summary, Anxa3 knockdown inhibited the growth, migration, invasion, and metastasis of LADC, decreased the activation of the MEK/ERK signaling pathway, and modulated the expression of MMP-2, E-cadherin, and N-cadherin.
[Mh] Termos MeSH primário: Adenocarcinoma/metabolismo
Adenocarcinoma/patologia
Anexina A3/metabolismo
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Sobrevivência Celular
Regulação para Baixo
Técnicas de Silenciamento de Genes
Seres Humanos
Sistema de Sinalização das MAP Quinases
Masculino
Camundongos Endogâmicos BALB C
Camundongos Nus
Invasividade Neoplásica
Metástase Neoplásica
Transdução de Sinais
Cicatrização
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.1.4.43 (Annexin A3)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE


  3 / 101 MEDLINE  
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[PMID]:27475959
[Au] Autor:Zhang Z; Kong Z; Zhu M; Lu W; Ni L; Bai Y; Lou Y
[Ad] Endereço:Department of Orthopaedic, Nanjing Children's Hospital Affiliated to Nanjing Medical University, 72 Guangzhou Road, Nanjing, 210008, Jiangsu, China.
[Ti] Título:Whole genome sequencing identifies ANXA3 and MTHFR mutations in a large family with an unknown equinus deformity associated genetic disorder.
[So] Source:Mol Biol Rep;43(10):1147-55, 2016 Oct.
[Is] ISSN:1573-4978
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to characterize a previously uncharacterized genetic disorder associated with equinus deformity in a large Chinese family at the genetic level. Blood samples were obtained and whole genome sequencing was performed. Differential gene variants were identified and potential impacts on protein structure were predicted. Based on the control sample, several diseases associated variants were identified and selected for further validation. One of the potential variants identified was a ANXA3 gene [chr4, c.C820T(p.R274*)] variant. Further bioinformatic analysis showed that the observed mutation could lead to a three-dimensional conformational change. Moreover, a MTHFR variant that is different from variants associated with clubfoot was also identified. Bioinformatic analysis showed that this mutation could alter the protein binding region. These findings imply that this uncharacterized genetic disorder is not clubfoot, despite sharing some similar symptoms. Furthermore, specific CNV profiles were identified in association with the diseased samples, thus further speaking to the complexity of this multigenerational disorder. This study examined a previously uncharacterized genetic disorder appearing similar to clubfoot and yet having distinct features. Following whole genome sequencing and comparative analysis, several differential gene variants were identified to enable a further distinction from clubfoot. It is hoped that these findings will provide further insight into this disorder and other similar disorders.
[Mh] Termos MeSH primário: Anexina A3/genética
Pé Equino/genética
Metilenotetra-Hidrofolato Redutase (NADPH2)/genética
Mutação
Análise de Sequência de DNA/métodos
[Mh] Termos MeSH secundário: Anexina A3/química
Grupo com Ancestrais do Continente Asiático/genética
Sítios de Ligação
China
Feminino
Estudos de Associação Genética
Predisposição Genética para Doença
Seres Humanos
Masculino
Metilenotetra-Hidrofolato Redutase (NADPH2)/química
Modelos Moleculares
Linhagem
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANXA3 protein, human); EC 1.5.1.20 (MTHFR protein, human); EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2)); EC 3.1.4.43 (Annexin A3)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160801
[St] Status:MEDLINE
[do] DOI:10.1007/s11033-016-4047-2


  4 / 101 MEDLINE  
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[PMID]:26475168
[Au] Autor:Takahashi H; Kaniwa N; Saito Y; Sai K; Hamaguchi T; Shirao K; Shimada Y; Matsumura Y; Ohtsu A; Yoshino T; Doi T; Takahashi A; Odaka Y; Okuyama M; Sawada J; Sakamoto H; Yoshida T
[Ad] Endereço:Graduate School of Horticulture, Chiba University, 648 Matsudo, Matsudo, Chiba, 271-8510, Japan. hiro.takahashi@chiba-u.jp.
[Ti] Título:Construction of possible integrated predictive index based on EGFR and ANXA3 polymorphisms for chemotherapy response in fluoropyrimidine-treated Japanese gastric cancer patients using a bioinformatic method.
[So] Source:BMC Cancer;15:718, 2015 Oct 16.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Variability in drug response between individual patients is a serious concern in medicine. To identify single-nucleotide polymorphisms (SNPs) related to drug response variability, many genome-wide association studies have been conducted. METHODS: We previously applied a knowledge-based bioinformatic approach to a pharmacogenomics study in which 119 fluoropyrimidine-treated gastric cancer patients were genotyped at 109,365 SNPs using the Illumina Human-1 BeadChip. We identified the SNP rs2293347 in the human epidermal growth factor receptor (EGFR) gene as a novel genetic factor related to chemotherapeutic response. In the present study, we reanalyzed these hypothesis-free genomic data using extended knowledge. RESULTS: We identified rs2867461 in annexin A3 (ANXA3) gene as another candidate. Using logistic regression, we confirmed that the performance of the rs2867461 + rs2293347 model was superior to those of the single factor models. Furthermore, we propose a novel integrated predictive index (iEA) based on these two polymorphisms in EGFR and ANXA3. The p value for iEA was 1.47 × 10(-8) by Fisher's exact test. Recent studies showed that the mutations in EGFR is associated with high expression of dihydropyrimidine dehydrogenase, which is an inactivating and rate-limiting enzyme for fluoropyrimidine, and suggested that the combination of chemotherapy with fluoropyrimidine and EGFR-targeting agents is effective against EGFR-overexpressing gastric tumors, while ANXA3 overexpression confers resistance to tyrosine kinase inhibitors targeting the EGFR pathway. CONCLUSIONS: These results suggest that the iEA index or a combination of polymorphisms in EGFR and ANXA3 may serve as predictive factors of drug response, and therefore could be useful for optimal selection of chemotherapy regimens.
[Mh] Termos MeSH primário: Anexina A3/genética
Receptor do Fator de Crescimento Epidérmico/genética
Neoplasias Gástricas/tratamento farmacológico
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Biologia Computacional/métodos
Resistência a Medicamentos Antineoplásicos/genética
Tratamento Farmacológico
Feminino
Fluoruracila/administração & dosagem
Fluoruracila/efeitos adversos
Estudo de Associação Genômica Ampla
Seres Humanos
Japão
Masculino
Mutação
Polimorfismo de Nucleotídeo Único
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.1.4.43 (Annexin A3); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151018
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-015-1721-z


  5 / 101 MEDLINE  
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[PMID]:26182056
[Au] Autor:Meadows SM; Cleaver O
[Ad] Endereço:Department of Cell and Molecular Biology, Tulane University, 2000 Percival Stern Hall, 6400 Freret St., New Orleans, LA, United States of America.
[Ti] Título:Annexin A3 Regulates Early Blood Vessel Formation.
[So] Source:PLoS One;10(7):e0132580, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Annexins are a large family of calcium binding proteins that associate with cell membrane phospholipids and are involved in various cellular processes including endocytosis, exocytosis and membrane-cytoskeletal organization. Despite studies on numerous Annexin proteins, the function of Annexin A3 (Anxa3) is largely unknown. Our studies identify Anxa3 as a unique marker of the endothelial and myeloid cell lineages of Xenopus laevis during development. Anxa3 transcripts are also detected in endothelial cells (ECs) of zebrafish and mouse embryos, suggesting an important evolutionary function during formation of blood vessels. Indeed, Anxa3 loss-of-function experiments in frog embryos reveal its critical role during the morphogenesis of early blood vessels, as angioblasts in MO injected embryos fail to form vascular cords. Furthermore, in vitro experiments in mammalian cells identify a role for Anxa3 in EC migration. Our results are the first to reveal an in vivo function for Anxa3 during vascular development and represent a previously unexplored aspect of annexin biology.
[Mh] Termos MeSH primário: Anexina A3/genética
Regulação da Expressão Gênica no Desenvolvimento
Neovascularização Fisiológica/genética
[Mh] Termos MeSH secundário: Animais
Anexina A3/antagonistas & inibidores
Anexina A3/metabolismo
Morte Celular
Linhagem Celular
Proliferação Celular
Embrião de Mamíferos
Embrião não Mamífero
Células Endoteliais/citologia
Células Endoteliais/metabolismo
Feminino
Masculino
Camundongos
Camundongos Transgênicos
Microinjeções
Morfolinos/genética
Morfolinos/metabolismo
Xenopus laevis
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Morpholinos); EC 3.1.4.43 (Annexin A3)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150717
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0132580


  6 / 101 MEDLINE  
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[PMID]:26095609
[Au] Autor:Tong M; Fung TM; Luk ST; Ng KY; Lee TK; Lin CH; Yam JW; Chan KW; Ng F; Zheng BJ; Yuan YF; Xie D; Lo CM; Man K; Guan XY; Ma S
[Ad] Endereço:Department of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong.
[Ti] Título:ANXA3/JNK Signaling Promotes Self-Renewal and Tumor Growth, and Its Blockade Provides a Therapeutic Target for Hepatocellular Carcinoma.
[So] Source:Stem Cell Reports;5(1):45-59, 2015 Jul 14.
[Is] ISSN:2213-6711
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Frequent tumor relapse in hepatocellular carcinoma (HCC) has been commonly attributed to the presence of residual cancer stem cells (CSCs) after conventional treatments. We have previously identified and characterized CD133 to mark a specific CSC subset in HCC. In the present study, we found endogenous and secretory annexin A3 (ANXA3) to play pivotal roles in promoting cancer and stem cell-like features in CD133+ liver CSCs through a dysregulated JNK pathway. Blockade of ANXA3 with an anti-ANXA3 monoclonal antibody in vitro as well as in human HCC xenograft models resulted in a significant reduction in tumor growth and self-renewal. Clinically, ANXA3 expression in HCC patient sera closely associated with aggressive clinical features. Our results suggest that ANXA3 can serve as a novel diagnostic biomarker and that the inhibition of ANXA3 may be a viable therapeutic option for the treatment of CD133+ liver-CSC-driven HCC.
[Mh] Termos MeSH primário: Anexina A3/genética
Antígenos CD/genética
Carcinoma Hepatocelular/genética
Glicoproteínas/genética
Neoplasias Hepáticas/genética
Células-Tronco Neoplásicas/metabolismo
Peptídeos/genética
[Mh] Termos MeSH secundário: Antígeno AC133
Adulto
Idoso
Anexina A3/biossíntese
Carcinoma Hepatocelular/patologia
Linhagem Celular Tumoral
Linhagem da Célula/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Fígado/metabolismo
Fígado/patologia
Neoplasias Hepáticas/patologia
Sistema de Sinalização das MAP Quinases/genética
Masculino
Meia-Idade
Proteínas de Neoplasias/biossíntese
Células-Tronco Neoplásicas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Antigens, CD); 0 (Glycoproteins); 0 (Neoplasm Proteins); 0 (PROM1 protein, human); 0 (Peptides); EC 3.1.4.43 (Annexin A3)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150623
[St] Status:MEDLINE


  7 / 101 MEDLINE  
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[PMID]:26093083
[Au] Autor:Zeidan B; Jackson TR; Larkin SE; Cutress RI; Coulton GR; Ashton-Key M; Murray N; Packham G; Gorgoulis V; Garbis SD; Townsend PA
[Ad] Endereço:Cancer Sciences Unit, University of Southampton, Southampton, UK.
[Ti] Título:Annexin A3 is a mammary marker and a potential neoplastic breast cell therapeutic target.
[So] Source:Oncotarget;6(25):21421-7, 2015 Aug 28.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Breast cancers are the most common cancer-affecting women; critically the identification of novel biomarkers for improving early detection, stratification and differentiation from benign tumours is important for the reduction of morbidity and mortality.To identify and functionally characterise potential biomarkers, we used mass spectrometry (MS) to analyse serum samples representing control, benign breast disease (BBD) and invasive breast cancer (IDC) patients. Complementary and multidimensional proteomic approaches were used to identify and validate novel serum markers.Annexin A3 (ANX A3) was found to be differentially expressed amongst different breast pathologies. The diagnostic value of serum ANX A3 was subsequently validated by ELISA in an independent serum set representing the three groups. Here, ANX A3 was significantly upregulated in the benign disease group sera compared with other groups (P < 0.0005).In addition, paired breast tissue immunostaining confirmed that ANX A3 was abundantly expressed in benign and to a lesser extent malignant neoplastic epithelium. Finally, we illustrated ANX A3 expression in cell culture lysates and conditioned media from neoplastic breast cell lines, and its role in neoplastic breast cell migration in vitro.This study confirms the novel role of ANX A3 as a mammary biomarker, regulator and therapeutic target.
[Mh] Termos MeSH primário: Anexina A3/metabolismo
Biomarcadores Tumorais/metabolismo
Neoplasias da Mama/metabolismo
Regulação Neoplásica da Expressão Gênica
[Mh] Termos MeSH secundário: Idoso
Mama/metabolismo
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Movimento Celular
Meios de Cultivo Condicionados
Ensaio de Imunoadsorção Enzimática
Epitélio/patologia
Feminino
Inativação Gênica
Seres Humanos
Imuno-Histoquímica
Células MCF-7
Espectrometria de Massas
Meia-Idade
Invasividade Neoplásica
Metástase Neoplásica
Proteômica
Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por Matriz
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Culture Media, Conditioned); EC 3.1.4.43 (Annexin A3)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150621
[St] Status:MEDLINE


  8 / 101 MEDLINE  
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[PMID]:25853334
[Au] Autor:Kuppe C; Gröne HJ; Ostendorf T; van Kuppevelt TH; Boor P; Floege J; Smeets B; Moeller MJ
[Ad] Endereço:Department of Internal Medicine II, Nephrology and Clinical Immunology, RWTH Aachen University Hospital, Aachen, Germany.
[Ti] Título:Common histological patterns in glomerular epithelial cells in secondary focal segmental glomerulosclerosis.
[So] Source:Kidney Int;88(5):990-8, 2015 Nov.
[Is] ISSN:1523-1755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Parietal epithelial cells (PECs) are involved in the development of sclerotic lesions in primary focal and segmental glomerulosclerosis (FSGS). Here, the role of PECs was explored in the more common secondary FSGS lesions in 68 patient biopsies, diagnosed with 11 different frequently or rarely encountered glomerular pathologies and additional secondary FSGS lesions. For each biopsy, one section was quadruple stained for PECs (ANXA3), podocytes (synaptopodin), PEC matrix (LKIV69), and Hoechst (nuclei), and a second was quadruple stained for activated PECs (CD44 and cytokeratin-19), PEC matrix, and nuclei. In all lesions, cellular adhesions (synechiae) between Bowman's capsule and the tuft were formed by cells expressing podocyte and/or PEC markers. Cells expressing PEC markers were detected in all FSGS lesions independent of the underlying glomerular disease and often stained positive for markers of activation. Small FSGS lesions, which were hardly identified on PAS sections previously, were detectable by immunofluorescent staining using PEC markers, potentially improving the diagnostic sensitivity to identify these lesions. Thus, similar patterns of cells expressing podocyte and/or PEC markers were found in the formation of secondary FSGS lesions independent of the underlying glomerular disease. Hence, our findings support the hypothesis that FSGS lesions follow a final cellular pathway to nephron loss that includes involvement of cells expressing PEC markers.
[Mh] Termos MeSH primário: Células Epiteliais/patologia
Glomerulosclerose Segmentar e Focal/patologia
Glomérulos Renais/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Anexina A3/análise
Cápsula Glomerular/patologia
Adesão Celular
Núcleo Celular/patologia
Claudina-1/análise
Células Epiteliais/química
Feminino
Imunofluorescência
Glomerulosclerose Segmentar e Focal/etiologia
Glomerulosclerose Segmentar e Focal/metabolismo
Seres Humanos
Receptores de Hialuronatos/análise
Queratina-19/análise
Glomérulos Renais/química
Masculino
Proteínas dos Microfilamentos/análise
Meia-Idade
Podócitos/química
Podócitos/patologia
Coloração e Rotulagem
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Claudin-1); 0 (Hyaluronan Receptors); 0 (Keratin-19); 0 (Microfilament Proteins); 0 (SYNPO protein, human); EC 3.1.4.43 (Annexin A3)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150409
[St] Status:MEDLINE
[do] DOI:10.1038/ki.2015.116


  9 / 101 MEDLINE  
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[PMID]:25780855
[Au] Autor:Tu C; Beharry KD; Shen X; Li J; Wang L; Aranda JV; Qu J
[Ad] Endereço:Department of Pharmaceutical Sciences, University at Buffalo, State University of New York, Buffalo, New York 14260, United States.
[Ti] Título:Proteomic profiling of the retinas in a neonatal rat model of oxygen-induced retinopathy with a reproducible ion-current-based MS1 approach.
[So] Source:J Proteome Res;14(5):2109-2120, 2015 May 01.
[Is] ISSN:1535-3907
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Investigation of the retina proteome during hypoxia-induced retinal neovascularization is valuable for understanding pathogenesis of retinopathy of prematurity (ROP). Here we employed a reproducible ion-current-based MS1 quantification approach (ICB) to explore the retinal proteomic changes in early stage of ROP in a rat model of oxygen-induced retinopathy (OIR). Retina proteins, which are rich in membrane proteins, were efficiently extracted by a detergent-cocktail and subjected to precipitation/on-pellet-digestion, followed by nano-LC-MS analysis on a 75-cm column with a 7-h gradient. The high reproducibility of sample preparation and chromatography separation enabled excellent peak alignment and contributed to the superior performance of ICB over parallel label-free approaches. In this study, sum-of-intensity with rejection was incorporated to determine the protein ratios. In total, 1325 unique protein groups were quantified from rat retinas (n = 4/group) with at least two distinct peptides at a protein FDR of 1%. Thirty-two significantly altered proteins were observed with confidence, and the elevated glial fibrillary acidic protein and decreased crystalline proteins in OIR retinas agree well with previous studies. Selected key alterations were further validated by Western blot analysis. Interestingly, Rab21/RhoA/ROCK2/moesin signaling pathway was found to be involved in retinal neovascularization of OIR. Moreover, highly elevated annexin A3, a potential angiogenic mediator, was observed in OIR retinas and may serve as a potential therapeutic target. In conclusion, reproducible ICB profiling enabled reliable discovery of many altered mediators and pathways in OIR retinas, thereby providing new insights into molecular mechanisms involved in pathogenesis of ROP.
[Mh] Termos MeSH primário: Proteínas do Olho/isolamento & purificação
Espectrometria de Massas/métodos
Proteoma/isolamento & purificação
Retina/química
Degeneração Retiniana/genética
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Anexina A3/genética
Anexina A3/isolamento & purificação
Anexina A3/metabolismo
Clusterina/genética
Clusterina/isolamento & purificação
Clusterina/metabolismo
Modelos Animais de Doenças
Proteínas do Olho/genética
Proteínas do Olho/metabolismo
Regulação da Expressão Gênica
Proteína Glial Fibrilar Ácida/genética
Proteína Glial Fibrilar Ácida/isolamento & purificação
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Proteínas de Membrana/genética
Proteínas de Membrana/isolamento & purificação
Proteínas de Membrana/metabolismo
Proteínas dos Microfilamentos/genética
Proteínas dos Microfilamentos/isolamento & purificação
Proteínas dos Microfilamentos/metabolismo
Neovascularização Patológica/genética
Oxigênio
Proteoma/genética
Proteoma/metabolismo
Ratos
Ratos Sprague-Dawley
Retina/metabolismo
Retina/patologia
Degeneração Retiniana/induzido quimicamente
Degeneração Retiniana/metabolismo
Degeneração Retiniana/patologia
Retinopatia da Prematuridade/genética
Retinopatia da Prematuridade/metabolismo
Retinopatia da Prematuridade/patologia
Fator de Transcrição STAT1/genética
Fator de Transcrição STAT1/isolamento & purificação
Fator de Transcrição STAT1/metabolismo
Proteínas rab de Ligação ao GTP/genética
Proteínas rab de Ligação ao GTP/isolamento & purificação
Proteínas rab de Ligação ao GTP/metabolismo
Quinases Associadas a rho/genética
Quinases Associadas a rho/isolamento & purificação
Quinases Associadas a rho/metabolismo
Proteína rhoA de Ligação ao GTP/genética
Proteína rhoA de Ligação ao GTP/isolamento & purificação
Proteína rhoA de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Clu protein, rat); 0 (Clusterin); 0 (Eye Proteins); 0 (Glial Fibrillary Acidic Protein); 0 (Membrane Proteins); 0 (Microfilament Proteins); 0 (Proteome); 0 (STAT1 Transcription Factor); 0 (Stat1 protein, rat); 144131-77-1 (moesin); EC 2.7.11.1 (ROCK2 protein, rat); EC 2.7.11.1 (rho-Associated Kinases); EC 3.1.4.43 (Annexin A3); EC 3.6.5.2 (rab GTP-Binding Proteins); EC 3.6.5.2 (rhoA GTP-Binding Protein); S88TT14065 (Oxygen)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150318
[St] Status:MEDLINE
[do] DOI:10.1021/pr501238m


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[PMID]:25267273
[Au] Autor:Pan QZ; Pan K; Wang QJ; Weng DS; Zhao JJ; Zheng HX; Zhang XF; Jiang SS; Lv L; Tang Y; Li YQ; He J; Liu Q; Chen CL; Zhang HX; Xia JC
[Ad] Endereço:Collaborative Innovation Center for Cancer Medicine, State Key Laboratory of Oncology in South China; Department of Biotherapy, Sun Yat-Sen University Cancer Center, Guangzhou, People's Republic of China.
[Ti] Título:Annexin A3 as a potential target for immunotherapy of liver cancer stem-like cells.
[So] Source:Stem Cells;33(2):354-66, 2015 Feb.
[Is] ISSN:1549-4918
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer stem-like cells/cancer-initiating cells (CSCs/CICs) are considered to represent a small population of cancer cells that is resistant to conventional cancer treatments and responsible for tumor recurrence and metastasis. The aim of this study was to establish CSC/CIC-targeting immunotherapy. In this study, we found that Annexin A3 (ANXA3) was preferentially expressed in CSCs/CICs derived from hepatocellular carcinoma (HCC) cells compared to non-CSCs/CICs. In HCC samples, high levels of ANXA3 correlated with expansion of CD133(+) tumor cells representing CSCs/CICs in HCC; the combination of high levels of ANXA3 and CD133 was associated with progression of HCC. Overexpression of ANXA3 increased the proportion of CD133(+) cells, enhancing their tumorigenicity. On the contrary, knockdown of ANXA3 decreased CD133(+) cells and inhibited tumorigenicity. The mechanistic study revealed that ANXA3-mediated maintenance of HCC CSCs/CICs activity was likely involved with the HIF1A/Notch pathway. Using ANXA3 as a target, ANXA3-transfected dendritic cells could induce more functionally active T cells and these effector T cells could superiorly kill CD133(+) HCC CSCs/CICs in vitro and in vivo. Taken together, our findings suggest that ANXA3 plays a role in HCC CSC/CIC maintenance, and that ANXA3 may represent a potential CSC/CIC-specific therapeutic target for improving the treatment of HCC.
[Mh] Termos MeSH primário: Anexina A3/imunologia
Imunoterapia
Neoplasias Hepáticas/terapia
Proteínas de Neoplasias/imunologia
Células-Tronco Neoplásicas/imunologia
[Mh] Termos MeSH secundário: Antígeno AC133
Animais
Anexina A3/genética
Antígenos CD/genética
Antígenos CD/imunologia
Células Dendríticas/imunologia
Células Dendríticas/patologia
Glicoproteínas/genética
Glicoproteínas/imunologia
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/imunologia
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/imunologia
Neoplasias Hepáticas/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Proteínas de Neoplasias/genética
Células-Tronco Neoplásicas/patologia
Peptídeos/genética
Peptídeos/imunologia
Receptores Notch/genética
Receptores Notch/imunologia
Linfócitos T/imunologia
Linfócitos T/patologia
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Antigens, CD); 0 (Glycoproteins); 0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Neoplasm Proteins); 0 (PROM1 protein, human); 0 (Peptides); 0 (Prom1 protein, mouse); 0 (Receptors, Notch); EC 3.1.4.43 (Annexin A3)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141001
[St] Status:MEDLINE
[do] DOI:10.1002/stem.1850



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