Base de dados : MEDLINE
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  1 / 145 MEDLINE  
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[PMID]:27650619
[Au] Autor:Zhang ZG; Chen JN; Wang YD; Gao JT; Jin Y
[Ad] Endereço:Department of Pathology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
[Ti] Título:The Role of Annexin A4 in Triple-Negative Breast Cancer Progression and Its Clinical Application.
[So] Source:Ann Clin Lab Sci;46(5):515-21, 2016 Sep.
[Is] ISSN:1550-8080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The expression of annexin A4 in triple-negative breast cancer (TNBC) remains unclear. In the present study, we investigated the expression of annexin A4 in TNBC tissues, as well as its relationship with clinicopathological and prognostic indicators, with an aim to assess its application value. METHODS: We adopted immunohistochemical and western blot to detect annexin A4 expression in TNBC and para-carcinoma tissues, and to explore the relationship between abnormal expression of annexin A4 and clinicopathological features of TNBC patients. RESULTS: The annexin A4 expression was significantly higher in TNBC tissues than in adjacent tissues. We analyzed the relationship between annexin A4 expression level and clinicopathological characteristics of TNBC patients. The results suggested that annexin A4 expression level was closely related to TNM stage, vascular involvement, lymphovascular invasion, and lymph node status of TNBC patients. The results survival analysis suggested upregulated expression of annexin A4 in TNBC patients with a shorter survival time. The results of a multifactor analysis showed that high annexin A4 expression rate was an independent predictive factor of the prognosis of the TNBC patients. CONCLUSIONS: The high annexin A4 expression indicates the poor prognosis of TNBC patients; thus, annexin A4 can be regarded as an important molecular marker in TNBC prognosis.
[Mh] Termos MeSH primário: Anexina A4/metabolismo
Progressão da Doença
Neoplasias de Mama Triplo Negativas/metabolismo
Neoplasias de Mama Triplo Negativas/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Feminino
Seres Humanos
Meia-Idade
Análise Multivariada
Prognóstico
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A4)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170113
[Lr] Data última revisão:
170113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160922
[St] Status:MEDLINE


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[PMID]:27485544
[Au] Autor:Liu W; Zeng L; Li N; Wang F; Jiang C; Guo F; Chen X; Su T; Xu C; Zhang S; Fang C
[Ad] Endereço:Department of Oral and Maxillofacial Surgery, Xiangya Hospital, Central South University, No. 88, Xiangya Road, Changsha, China.
[Ti] Título:Quantitative proteomic analysis for novel biomarkers of buccal squamous cell carcinoma arising in background of oral submucous fibrosis.
[So] Source:BMC Cancer;16:584, 2016 08 02.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In South and Southeast Asian, the majority of buccal squamous cell carcinoma (BSCC) can arise from oral submucous fibrosis (OSF). BSCCs develop in OSF that are often not completely resected, causing local relapse. The aim of our study was to find candidate protein biomarkers to detect OSF and predict prognosis in BSCCs by quantitative proteomics approaches. METHODS: We compared normal oral mucosa (NBM) and paired biopsies of BSCC and OSF by quantitative proteomics using isobaric tags for relative and absolute quantification (iTRAQ) to discover proteins with differential expression. Gene Ontology and KEGG networks were analyzed. The prognostic value of biomarkers was evaluated in 94 BSCCs accompanied with OSF. Significant associations were assessed by Kaplan-Meier survival and Cox-proportional hazards analysis. RESULTS: In total 30 proteins were identified with significantly different expression (false discovery rate < 0.05) among three tissues. Two consistently upregulated proteins, ANXA4 and FLNA, were validated. The disease-free survival was negatively associated with the expression of ANXA4 (hazard ratio, 3.4; P = 0.000), FLNA (hazard ratio, 2.1; P = 0.000) and their combination (hazard ratio, 8.8; P = 0.002) in BSCCs. CONCLUSION: The present study indicates that iTRAQ quantitative proteomics analysis for tissues of BSCC and OSF is a reliable strategy. A significantly up-regulated ANXA4 and FLNA could be not only candidate biomarkers for BSCC prognosis but also potential targets for its therapy.
[Mh] Termos MeSH primário: Anexina A4/metabolismo
Carcinoma de Células Escamosas/metabolismo
Filaminas/metabolismo
Neoplasias Bucais/metabolismo
Fibrose Oral Submucosa/patologia
Proteômica/métodos
[Mh] Termos MeSH secundário: Adulto
Ásia
Biomarcadores/metabolismo
Carcinoma de Células Escamosas/patologia
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Meia-Idade
Neoplasias Bucais/patologia
Fibrose Oral Submucosa/metabolismo
Prognóstico
Modelos de Riscos Proporcionais
Mapas de Interação de Proteínas
Análise de Sobrevida
Espectrometria de Massas em Tandem
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Annexin A4); 0 (Biomarkers); 0 (FLNA protein, human); 0 (Filamins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160804
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-016-2650-1


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[PMID]:27402115
[Au] Autor:Choi CH; Chung JY; Chung EJ; Sears JD; Lee JW; Bae DS; Hewitt SM
[Ad] Endereço:Experimental Pathology Laboratory, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, MSC 1500, Bethesda, MD, 20892, USA.
[Ti] Título:Prognostic significance of annexin A2 and annexin A4 expression in patients with cervical cancer.
[So] Source:BMC Cancer;16:448, 2016 07 11.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The annexins (ANXs) have diverse roles in tumor development and progression, however, their clinical significance in cervical cancer has not been elucidated. The present study was to investigate the clinical significance of annexin A2 (ANXA2) and annexin A4 (ANXA4) expression in cervical cancer. METHODS: ANXA2 and ANXA4 immunohistochemical staining were performed on a cervical cancer tissue microarray consisting of 46 normal cervical epithelium samples and 336 cervical cancer cases and compared the data with clinicopathological variables, including the survival of cervical cancer patients. RESULTS: ANXA2 expression was lower in cancer tissue (p = 0.002), whereas ANXA4 staining increased significantly in cancer tissues (p < 0.001). ANXA2 expression was more prominent in squamous cell carcinoma (p < 0.001), whereas ANXA4 was more highly expressed in adeno/adenosquamous carcinoma (p < 0.001). ANXA2 overexpression was positively correlated with advanced cancer phenotypes, whereas ANXA4 expression was associated with resistance to radiation with or without chemotherapy (p = 0.029). Notably, high ANXA2 and ANXA4 expression was significantly associated with shorter disease-free survival (p = 0.004 and p = 0.033, respectively). Multivariate analysis indicated that ANXA2+ (HR = 2.72, p = 0.003) and ANXA2+/ANXA4+ (HR = 2.69, p = 0.039) are independent prognostic factors of disease-free survival in cervical cancer. Furthermore, a random survival forest model using combined ANXA2, ANXA4, and clinical variables resulted in improved predictive power (mean C-index, 0.76) compared to that of clinical-variable-only models (mean C-index, 0.70) (p = 0.006). CONCLUSIONS: These findings indicate that detecting ANXA2 and ANXA4 expression may aid the evaluation of cervical carcinoma prognosis.
[Mh] Termos MeSH primário: Anexina A2/metabolismo
Anexina A4/metabolismo
Carcinoma Adenoescamoso/patologia
Carcinoma de Células Escamosas/patologia
Neoplasias do Colo do Útero/patologia
[Mh] Termos MeSH secundário: Adulto
Biomarcadores Tumorais/metabolismo
Carcinoma Adenoescamoso/mortalidade
Carcinoma de Células Escamosas/mortalidade
Intervalo Livre de Doença
Feminino
Seres Humanos
Imuno-Histoquímica
Meia-Idade
Prognóstico
Análise de Sobrevida
Análise Serial de Tecidos
Neoplasias do Colo do Útero/mortalidade
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (ANXA2 protein, human); 0 (Annexin A2); 0 (Annexin A4); 0 (Biomarkers, Tumor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160713
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-016-2459-y


  4 / 145 MEDLINE  
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[PMID]:27178140
[Au] Autor:Kreft S; Klatt AR; Straßburger J; Pöschl E; Flower RJ; Eming S; Reutelingsperger C; Brisson A; Brachvogel B
[Ti] Título:Skin Wound Repair Is Not Altered in the Absence of Endogenous AnxA1 or AnxA5, but Pharmacological Concentrations of AnxA4 and AnxA5 Inhibit Wound Hemostasis.
[So] Source:Cells Tissues Organs;201(4):287-98, 2016.
[Is] ISSN:1422-6421
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Skin injury induces the cell surface exposure of phosphatidylserine (PS) on damaged and dying cells to activate coagulation and repair processes. Annexins can bind to PS and may modulate the healing response. Here, we determine the relevance of annexins for skin wound healing using AnxA1- and AnxA5-deficient mice and recombinant annexins with distinct PS binding properties. Wound inflammation, closure and the formation of granulation tissue were not altered in AnxA1- or AnxA5-deficient mice or after increasing AnxA5 serum concentrations (100 nM) in wild-type mice. Increased serum concentrations (1 µM) of AnxA5 induced massive bleeding, but wound hemostasis was not delayed by AnxA1. Both annexins interact with PS, but only AnxA5 can form 2-dimensional (2D) arrays on the cell surface. The injection of an AnxA5 mutant that binds to PS but lacks the ability of 2D array formation failed to induce bleeding. 2D lattice-forming AnxA4, with high affinity to PS also caused bleeding, while hemostasis was not affected by AnxA8 with low affinity or the AnxA8 mutant with medium affinity for PS and the lack of 2D formation. Increased concentrations of AnxA4 and AnxA5 also delayed coagulation pathway activation in vitro. This effect was attenuated for the AnxA5 mutant as well as for AnxA1 and AnxA8. In conclusion, endogenous AnxA1 and AnxA5 are dispensable for wound hemostasis and repair, but pharmacologically excessive concentrations of AnxA4 and AnxA5 inhibit hemostasis in skin wounds.
[Mh] Termos MeSH primário: Anexina A1/deficiência
Anexina A4/farmacologia
Anexina A5/farmacologia
Hemorragia/tratamento farmacológico
Hemostasia/efeitos dos fármacos
Cicatrização/fisiologia
[Mh] Termos MeSH secundário: Animais
Anexina A1/genética
Anexina A5/deficiência
Anexina A5/genética
Citometria de Fluxo
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fosfatidilserinas/metabolismo
Tempo de Protrombina
Ratos
Proteínas Recombinantes/farmacologia
Pele/lesões
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Annexin A1); 0 (Annexin A4); 0 (Annexin A5); 0 (Phosphatidylserines); 0 (Recombinant Proteins); 0 (annexin A1, mouse)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160515
[St] Status:MEDLINE
[do] DOI:10.1159/000445106


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[PMID]:26982031
[Au] Autor:Barbone D; Van Dam L; Follo C; Jithesh PV; Zhang SD; Richards WG; Bueno R; Fennell DA; Broaddus VC
[Ad] Endereço:Department of Medicine, Pulmonary, San Francisco General Hospital, University of California San Francisco, San Francisco, California, United States of America.
[Ti] Título:Analysis of Gene Expression in 3D Spheroids Highlights a Survival Role for ASS1 in Mesothelioma.
[So] Source:PLoS One;11(3):e0150044, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To investigate the underlying causes of chemoresistance in malignant pleural mesothelioma, we have studied mesothelioma cell lines as 3D spheroids, which acquire increased chemoresistance compared to 2D monolayers. We asked whether the gene expression of 3D spheroids would reveal mechanisms of resistance. To address this, we measured gene expression of three mesothelioma cell lines, M28, REN and VAMT, grown as 2D monolayers and 3D spheroids. A total of 209 genes were differentially expressed in common by the three cell lines in 3D (138 upregulated and 71 downregulated), although a clear resistance pathway was not apparent. We then compared the list of 3D genes with two publicly available datasets of gene expression of 56 pleural mesotheliomas compared to normal tissues. Interestingly, only three genes were increased in both 3D spheroids and human tumors: argininosuccinate synthase 1 (ASS1), annexin A4 (ANXA4) and major vault protein (MVP); of these, ASS1 was the only consistently upregulated of the three genes by qRT-PCR. To measure ASS1 protein expression, we stained 2 sets of tissue microarrays (TMA): one with 88 pleural mesothelioma samples and the other with additional 88 pleural mesotheliomas paired with matched normal tissues. Of the 176 tumors represented on the two TMAs, ASS1 was expressed in 87 (50%; staining greater than 1 up to 3+). For the paired samples, ASS1 expression in mesothelioma was significantly greater than in the normal tissues. Reduction of ASS1 expression by siRNA significantly sensitized mesothelioma spheroids to the pro-apoptotic effects of bortezomib and of cisplatin plus pemetrexed. Although mesothelioma is considered by many to be an ASS1-deficient tumor, our results show that ASS1 is elevated at the mRNA and protein levels in mesothelioma 3D spheroids and in human pleural mesotheliomas. We also have uncovered a survival role for ASS1, which may be amenable to targeting to undermine mesothelioma multicellular resistance.
[Mh] Termos MeSH primário: Argininossuccinato Sintase/metabolismo
Sobrevivência Celular
Regulação Enzimológica da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Mesotelioma/genética
Esferoides Celulares
[Mh] Termos MeSH secundário: Anexina A4/metabolismo
Linhagem Celular Tumoral
Seres Humanos
Mesotelioma/patologia
Partículas de Ribonucleoproteínas em Forma de Abóbada/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Annexin A4); 0 (Vault Ribonucleoprotein Particles); 0 (major vault protein); EC 6.3.4.5 (Argininosuccinate Synthase)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160324
[Lr] Data última revisão:
160324
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160317
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0150044


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[PMID]:26779633
[Au] Autor:Chen W; Chen L; Cai Z; Liang D; Zhao B; Zeng Y; Liu X; Liu J
[Ad] Endereço:Liver Disease Center, The First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, People's Republic of China.
[Ti] Título:Overexpression of annexin A4 indicates poor prognosis and promotes tumor metastasis of hepatocellular carcinoma.
[So] Source:Tumour Biol;37(7):9343-55, 2016 Jul.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The prognosis of hepatocellular carcinoma (HCC) after surgical resection remains unsatisfactory for the majority of HCC patients who developed early recurrence or metastasis. There is still a lack of reliable biomarkers that can be used to predict the possibility of recurrence/metastasis in HCC patients after operation. In the current study, annexin A4, a calcium-dependent phospholipid-binding protein, has been found to be significantly elevated in HCC patients with early recurrence/metastasis, and had a strong correlation with portal vein tumor thrombosis (p = 0.03) and advanced BCLC stage (p = 0.002). Cox proportional hazards regression analysis revealed that annexin A4 was an independent prognostic predictor for both early recurrence/metastasis (HR = 1.519, p = 0.032) and overall survival (HR = 1.827, p = 0.009) after surgical resection. Meanwhile, Kaplan-Meier analysis showed that Patients with high-expression levels of annexin A4 had higher recurrence rate and shorter overall survival than those with low expression (log-rank test, p < 0.001). Furthermore, in vitro studies have demonstrated that overexpression of annexin A4 facilitated HCC cell migration and invasion via regulating epithelial-mesenchymal transition (EMT). In conclusion, annexin A4 has played important roles in the progression of HCC, and might act as a potential prognostic biomarker for HCC.
[Mh] Termos MeSH primário: Anexina A4/metabolismo
Biomarcadores Tumorais/metabolismo
Carcinoma Hepatocelular/secundário
Neoplasias Hepáticas/patologia
Recidiva Local de Neoplasia/patologia
[Mh] Termos MeSH secundário: Anexina A4/genética
Apoptose
Biomarcadores Tumorais/genética
Western Blotting
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/metabolismo
Movimento Celular
Proliferação Celular
Feminino
Seguimentos
Seres Humanos
Técnicas Imunoenzimáticas
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/metabolismo
Masculino
Meia-Idade
Invasividade Neoplásica
Recidiva Local de Neoplasia/genética
Recidiva Local de Neoplasia/metabolismo
Estadiamento de Neoplasias
Prognóstico
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Taxa de Sobrevida
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Annexin A4); 0 (Biomarkers, Tumor); 0 (RNA, Messenger)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160119
[St] Status:MEDLINE
[do] DOI:10.1007/s13277-016-4823-6


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[PMID]:26675575
[Au] Autor:Mu T; Li H; Wang J; Yao Y; Shen D
[Ad] Endereço:Department of Obstetrics and Gynecology, Peking University People's Hospital, Beijing 100044, China.
[Ti] Título:[Pathologic features of fallopian tubal fimbriae in patients with endometrial serous carcinoma].
[So] Source:Zhonghua Fu Chan Ke Za Zhi;50(10):757-61, 2015 Oct.
[Is] ISSN:0529-567X
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To discuss the potential relationship between endometrial serous carcinoma (ESC) and tubal epithelial lesions by pathologic examination of fallopian tubes with ESC. METHODS: A total of 30 cases of typical ESC were reexamined and chosen by the pathologist. In each case, bilateral fallopian tubes were submitted to examination of pathologic morphology and immunostaining for p53, annexin IV (ANX-IV), human epidermal growth factor receptor 2 (HER2)/neu, and high-mobility group protein A2 (HMGA2). RESULTS: Fallopian tubal epithelial lesions were found in 15 cases, including 9 cases tubal serous carcinoma, 2 cases serous tubal intraepithelial carcinoma (STIC) and 2 cases epithelial hyperplasia. Both sides of tubal serous carcinoma and STIC were found in 1 case. The results showed the positive expression for p53 in 26 (87%) out of 30 endometrial malignant specimens tissues and 9 (30%) tubal tissues samples (P > 0.05). Twenty-five (83%) endometrial malignant specimens tissues and 6 (20%) tubal tissues samples showed the positive expression of ANX-IV. Twenty-one (70%) endometrial malignant tissues and 7 (23%) tubal tissues showed the positive expression of HER2/neu. Twenty-five (83%) endometrial malignant tissues and 6 (20%) tubal tissues showed the positive expression of HMGA2. While, there were significant differences among the expression of three proteins between endometrium and the fallopian tube site (all P < 0.05). CONCLUSIONS: STIC may be associated with the occurrence of ESC. The expression of p53 was positively correlated between the fallopian tube and the endometrium. ANX-IV, HER2/neu and HMGA2 were extensively expressed in ESC.
[Mh] Termos MeSH primário: Cistadenocarcinoma Seroso/patologia
Tumores do Estroma Endometrial/patologia
Neoplasias das Tubas Uterinas/patologia
Tubas Uterinas/patologia
[Mh] Termos MeSH secundário: Animais
Anexina A4
Carcinoma in Situ
Endométrio
Feminino
Seres Humanos
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A4)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:151217
[Lr] Data última revisão:
151217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151218
[St] Status:MEDLINE


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[PMID]:26048190
[Au] Autor:Wei B; Guo C; Liu S; Sun MZ
[Ad] Endereço:Department of Biotechnology, Dalian Medical University, Dalian 116044, China.
[Ti] Título:Annexin A4 and cancer.
[So] Source:Clin Chim Acta;447:72-8, 2015 Jul 20.
[Is] ISSN:1873-3492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Annexin A4 (Anxa4) is one of the Ca(2+)-regulated and phospholipid-binding annexin superfamily proteins. Anxa4 has a potential role in diagnosis, prognosis, and treatment of certain cancers. Studies indicate that Anxa4 up-regulation promotes the progression of tumor and chemoresistance of colorectal cancer (CRC), esophageal squamous cell carcinoma (ESCC), endometrial carcinoma (EC), gastric cancer (GC), chemoresistant lung cancer (LC), malignant mesothelioma (MM), renal cell carcinoma (RCC), ovarian clear cell carcinoma (OCCC), cholangiocarcinoma, hepatocellular carcinoma (HCC), breast cancer (BC), and laryngeal cancer. Interestingly, Anxa4 also might specifically function as a tumor suppressor for prostate cancer (PCa) and have a paradoxical role for pancreatic cancer (PCC). Differential expression of Anxa4 may distinguish major salivary gland tumor (MSGT) from thyroid cancer. In addition, its differential expression was linked to Sirt1-induced cisplatin resistance of oral squamous cell carcinoma (OSCC) and miR-7-induced migration and invasion inhibition of glioma. This current review summarizes and discusses the clinical significance of Anxa4 in cancer as well as its potential mechanisms of action. It may provide new integrative understanding for future studies on the exact role of Anxa4 in cancer.
[Mh] Termos MeSH primário: Anexina A4/metabolismo
Neoplasias/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Annexin A4)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150630
[Lr] Data última revisão:
150630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150607
[St] Status:MEDLINE


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[PMID]:26023182
[Au] Autor:Heinick A; Husser X; Himmler K; Kirchhefer U; Nunes F; Schulte JS; Seidl MD; Rolfes C; Dedman JR; Kaetzel MA; Gerke V; Schmitz W; Müller FU
[Ad] Endereço:*Institute of Pharmacology and Toxicology, Institute of Medical Biochemistry, Center for Molecular Biology of Inflammation, and Interdisciplinary Clinical Research Center, University of Münster, Münster, Germany; and Department of Genome Science, University of Cincinnati Genome Research Institute, C
[Ti] Título:Annexin A4 is a novel direct regulator of adenylyl cyclase type 5.
[So] Source:FASEB J;29(9):3773-87, 2015 Sep.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Annexin A4 (AnxA4), a Ca(2+)- and phospholipid-binding protein, is up-regulated in the human failing heart. In this study, we examined the impact of AnxA4 on ß-adrenoceptor (ß-AR)/cAMP-dependent signal transduction. Expression of murine AnxA4 in human embryonic kidney (HEK)293 cells dose-dependently inhibited cAMP levels after direct stimulation of adenylyl cyclases (ACs) with forskolin (FSK), as determined with an exchange protein activated by cAMP-Förster resonance energy transfer (EPAC-FRET) sensor and an ELISA (control vs. +AnxA4: 1956 ± 162 vs. 1304 ± 185 fmol/µg protein; n = 8). Disruption of the anxA4 gene led to a consistent increase in intracellular cAMP levels in isolated adult mouse cardiomyocytes, with heart-directed expression of the EPAC-FRET sensor, stimulated with FSK, and as determined by ELISA, also in mouse cardiomyocytes stimulated with the ß-AR agonist isoproterenol (ISO) (anxA4a(+/+) vs. anxA4a(-/-): 5.1 ± 0.3 vs. 6.7 ± 0.6 fmol/µg protein) or FSK (anxA4a(+/+) vs. anxA4a(-/-): 1891 ± 238 vs. 2796 ± 343 fmol/µg protein; n = 9-10). Coimmunoprecipitation experiments in HEK293 cells revealed a direct interaction of murine AnxA4 with human membrane-bound AC type 5 (AC5). As a functional consequence of AnxA4-mediated AC inhibition, AnxA4 inhibited the FSK-induced transcriptional activation mediated by the cAMP response element (CRE) in reporter gene studies (10-fold vs. control; n = 4 transfections) and reduced the FSK-induced phosphorylation of the CRE-binding protein (CREB) measured on Western blots (control vs. +AnxA4: 150 ± 17% vs. 105 ± 10%; n = 6) and by the use of the indicator of CREB activation caused by phosphorylation (ICAP)-FRET sensor, indicating CREB phosphorylation. Inactivation of AnxA4 in anxA4a(-/-) mice was associated with an increased cardiac response to ß-AR stimulation. Together, these results suggest that AnxA4 is a novel direct negative regulator of AC5, adding a new facet to the functions of annexins.
[Mh] Termos MeSH primário: Adenilil Ciclases/metabolismo
Anexina A4/metabolismo
Membrana Celular/metabolismo
Miocárdio/metabolismo
Miócitos Cardíacos/metabolismo
[Mh] Termos MeSH secundário: Adenilil Ciclases/genética
Animais
Anexina A4/genética
Proteína de Ligação a CREB/genética
Proteína de Ligação a CREB/metabolismo
Membrana Celular/genética
Células HEK293
Seres Humanos
Camundongos
Camundongos Knockout
Fosforilação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Annexin A4); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (CREBBP protein, human); EC 2.3.1.48 (Crebbp protein, mouse); EC 4.6.1.1 (Adenylyl Cyclases); EC 4.6.1.1 (adenylyl cyclase type V)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150530
[St] Status:MEDLINE
[do] DOI:10.1096/fj.14-269837


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[PMID]:25825397
[Au] Autor:Atkinson C; Qiao F; Yang X; Zhu P; Reaves N; Kulik L; Goddard M; Holers VM; Tomlinson S
[Ad] Endereço:From Department of Microbiology and Immunology, Medical University of South Carolina, Charleston (CA., F.Q., X.Y., P.Z., N.R., S.T.); Department of Medicine and Immunology, University of Colorado Denver, Aurora (L.K., V.M.H.); Department of Pathology, Papworth Hospital, Cambridgeshire, UK (M.G.); an
[Ti] Título:Targeting pathogenic postischemic self-recognition by natural IgM to protect against posttransplantation cardiac reperfusion injury.
[So] Source:Circulation;131(13):1171-80, 2015 Mar 31.
[Is] ISSN:1524-4539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Natural IgM antibodies represent a class of innate pattern recognition receptors that recognize danger-associated molecular patterns expressed on stressed or dying cells. They play important roles in tissue homeostasis by disposing of prenecrotic cells and suppressing inflammation. However, ischemic insult leads to a pathogenic level of IgM binding and complement activation, resulting in inflammation and injury. We investigate the role of self-reactive IgM in the unique setting of transplantation where the donor organ undergoes both cold and warm ischemia and global ischemic insult. METHODS AND RESULTS: By transplanting hearts from wild-type donor mice into antibody-deficient mice reconstituted with specific self-reactive IgM monoclonal antibodies, we identified neoepitopes expressed after transplantation and demonstrated a key role for IgM recognition of these epitopes in graft injury. With this information, we developed and characterized a therapeutic strategy that exploited the postischemia recognition system of natural antibodies. On the basis of neoepitope identification, we constructed an anti-annexin IV single-chain antibody (scFv) and an scFv linked to Crry, an inhibitor of C3 activation (scFv-Crry). In an allograft transplantation model in which recipients contain a full natural antibody repertoire, both constructs blocked graft IgM binding and complement activation and significantly reduced graft inflammation and injury. Furthermore, scFv-Crry specifically targeted to the transplanted heart and, unlike complement deficiency, did not affect immunity to infection, an important consideration for immunosuppressed transplant recipients. CONCLUSIONS: We identified pathophysiologically important epitopes expressed within the heart after transplantation and described a novel translatable strategy for targeted complement inhibition that has several advantages over currently available approaches.
[Mh] Termos MeSH primário: Anticorpos Biespecíficos/uso terapêutico
Anticorpos Monoclonais/uso terapêutico
Transplante de Coração/efeitos adversos
Imunoglobulina M/uso terapêutico
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Reperfusão Miocárdica/efeitos adversos
Receptores de Complemento/uso terapêutico
Tolerância a Antígenos Próprios/imunologia
Anticorpos de Cadeia Única/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Anexina A4/imunologia
Anticorpos Biespecíficos/genética
Anticorpos Biespecíficos/imunologia
Anticorpos Monoclonais/genética
Anticorpos Monoclonais/imunologia
Ativação do Complemento
Epitopos/imunologia
Genes Sintéticos
Proteínas de Homeodomínio/genética
Imunoglobulina M/deficiência
Imunoglobulina M/genética
Imunoglobulina M/imunologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Traumatismo por Reperfusão Miocárdica/imunologia
Miocárdio/imunologia
Especificidade de Órgãos
Fosfolipídeos/imunologia
Receptores de Complemento/genética
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/imunologia
Proteínas Recombinantes de Fusão/uso terapêutico
Anticorpos de Cadeia Única/genética
Anticorpos de Cadeia Única/imunologia
Tolerância ao Transplante
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Annexin A4); 0 (Antibodies, Bispecific); 0 (Antibodies, Monoclonal); 0 (Crry protein, mouse); 0 (Epitopes); 0 (Homeodomain Proteins); 0 (Immunoglobulin M); 0 (Phospholipids); 0 (Receptors, Complement); 0 (Recombinant Fusion Proteins); 0 (Single-Chain Antibodies); 128559-51-3 (RAG-1 protein)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150401
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCULATIONAHA.114.010482



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