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[PMID]:28946285
[Au] Autor:Mattison CP; Malveira Cavalcante J; Izabel Gallão M; Sousa de Brito E
[Ad] Endereço:Agricultural Research Service, United States Department of Agriculture, New Orleans, LA 70124, USA. Electronic address: chris.mattison@ars.usda.gov.
[Ti] Título:Effects of industrial cashew nut processing on anacardic acid content and allergen recognition by IgE.
[So] Source:Food Chem;240:370-376, 2018 Feb 01.
[Is] ISSN:0308-8146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cashew nuts are important both nutritionally and industrially, but can also cause food allergies in some individuals. The present study aimed to assess the effect(s) of industrial processing on anacardic acids and allergens present in cashew nuts. Sample analyses were performed using liquid chromatography coupled with mass spectrometry, SDS-PAGE and immunoassay. The anacardic acid concentration ranged from 6.2 to 82.6mg/g during processing, and this variation was attributed to cashew nut shell liquid incorporation during storage and humidification. Dehydrated and selected samples did not significantly differ in anacardic acid content, having values similar to the raw sample. SDS-PAGE and immunoassay analysis with rabbit polyclonal sera and human IgE indicated only minor differences in protein solubility and antibody binding following processing steps. The findings indicate that appreciable amounts of anacardic acid remain in processed nuts, and that changes to cashew allergens during industrial processing may only mildly affect antibody recognition.
[Mh] Termos MeSH primário: Anacardium
[Mh] Termos MeSH secundário: Alérgenos
Ácidos Anacárdicos
Animais
Seres Humanos
Imunoglobulina E
Nozes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (Anacardic Acids); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE


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[PMID]:28886127
[Au] Autor:Schultz DJ; Muluhngwi P; Alizadeh-Rad N; Green MA; Rouchka EC; Waigel SJ; Klinge CM
[Ad] Endereço:Department of Biology, University of Louisville, Louisville, Kentucky, United States of America.
[Ti] Título:Genome-wide miRNA response to anacardic acid in breast cancer cells.
[So] Source:PLoS One;12(9):e0184471, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs are biomarkers and potential therapeutic targets for breast cancer. Anacardic acid (AnAc) is a dietary phenolic lipid that inhibits both MCF-7 estrogen receptor α (ERα) positive and MDA-MB-231 triple negative breast cancer (TNBC) cell proliferation with IC50s of 13.5 and 35 µM, respectively. To identify potential mediators of AnAc action in breast cancer, we profiled the genome-wide microRNA transcriptome (microRNAome) in these two cell lines altered by the AnAc 24:1n5 congener. Whole genome expression profiling (RNA-seq) and subsequent network analysis in MetaCore Gene Ontology (GO) algorithm was used to characterize the biological pathways altered by AnAc. In MCF-7 cells, 69 AnAc-responsive miRNAs were identified, e.g., increased let-7a and reduced miR-584. Fewer, i.e., 37 AnAc-responsive miRNAs were identified in MDA-MB-231 cells, e.g., decreased miR-23b and increased miR-1257. Only two miRNAs were increased by AnAc in both cell lines: miR-612 and miR-20b; however, opposite miRNA arm preference was noted: miR-20b-3p and miR-20b-5p were upregulated in MCF-7 and MDA-MB-231, respectively. miR-20b-5p target EFNB2 transcript levels were reduced by AnAc in MDA-MB-231 cells. AnAc reduced miR-378g that targets VIM (vimentin) and VIM mRNA transcript expression was increased in AnAc-treated MCF-7 cells, suggesting a reciprocal relationship. The top three enriched GO terms for AnAc-treated MCF-7 cells were B cell receptor signaling pathway and ribosomal large subunit biogenesis and S-adenosylmethionine metabolic process for AnAc-treated MDA-MB-231 cells. The pathways modulated by these AnAc-regulated miRNAs suggest that key nodal molecules, e.g., Cyclin D1, MYC, c-FOS, PPARγ, and SIN3, are targets of AnAc activity.
[Mh] Termos MeSH primário: Ácidos Anacárdicos/farmacologia
Neoplasias da Mama/genética
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Estudo de Associação Genômica Ampla
MicroRNAs/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Sobrevivência Celular/genética
Análise por Conglomerados
Feminino
Perfilação da Expressão Gênica
Redes Reguladoras de Genes
Seres Humanos
Interferência de RNA
RNA Mensageiro/genética
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anacardic Acids); 0 (MicroRNAs); 0 (RNA, Messenger); 18654-18-7 (anacardic acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184471


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[PMID]:28285020
[Au] Autor:Cunha AG; Brito ES; Moura CF; Ribeiro PR; Miranda MR
[Ad] Endereço:Federal University of Ceará. Dept. of Biochemistry and Molecular Biology, Campus Pici,Av. Mister Hull 2297 Bl. 907, Fortaleza, CE, CEP 60440-554, Brazil.
[Ti] Título:UPLC-qTOF-MS/MS-based phenolic profile and their biosynthetic enzyme activity used to discriminate between cashew apple (Anacardium occidentale L.) maturation stages.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1051:24-32, 2017 Apr 15.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cashew immature and ripe peduncles (Anacardium occidentale L.) from orange- and red-colored clones CCP 76 and BRS 189, respectively, were prepared as juice or fibrous fraction and submitted to UPLC-MS analyses, while the soluble fraction was also submitted to enzymatic evaluation. Cinnamoyl glucoside was present in ripe juice samples from both cashew clones, while monogalloyl diglucoside and digalloyl glucoside were present in immature juice samples from both cashew clones. Four compounds were found at immature fiber of both clones, anacardic acids (1, 2, 3) and GA . The phenolic biosynthetic pathway was evaluated in juice samples and phenylalanine ammonia-lyase activity decreased significantly during the development, although it was much higher in ripe CCP 76. UDP-glycosyltransferases activity differed between clones, however its product cinnamoyl glucoside was a possible chemical marker of ripe juice samples from both clones. Flavonol synthase showed the highest specific activity in both cashew clones and its product, flavonols were identified in cashew apple at immature and ripe stages.
[Mh] Termos MeSH primário: Ácidos Anacárdicos/análise
Anacardium/enzimologia
Anacardium/crescimento & desenvolvimento
Frutas/enzimologia
Frutas/crescimento & desenvolvimento
Glucosídeos/análise
Fenóis/análise
[Mh] Termos MeSH secundário: Ácidos Anacárdicos/metabolismo
Anacardium/química
Anacardium/metabolismo
Vias Biossintéticas
Cromatografia Líquida de Alta Pressão
Frutas/química
Frutas/metabolismo
Glucosídeos/metabolismo
Glucuronosiltransferase/metabolismo
Oxirredutases/metabolismo
Fenóis/metabolismo
Fenilalanina Amônia-Liase/metabolismo
Proteínas de Plantas/metabolismo
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anacardic Acids); 0 (Glucosides); 0 (Phenols); 0 (Plant Proteins); EC 1.- (Oxidoreductases); EC 1.3.- (flavonol synthase); EC 2.4.1.17 (Glucuronosyltransferase); EC 4.3.1.24 (Phenylalanine Ammonia-Lyase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170313
[St] Status:MEDLINE


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[PMID]:28237615
[Au] Autor:Kim MK; Kim EJ; Cheng Y; Shin MH; Oh JH; Lee DH; Chung JH
[Ad] Endereço:Department of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea; Laboratory of Cutaneous Aging Research, Biomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea; Institute of Human-Environment Interface Biology, Seoul National Un
[Ti] Título:Inhibition of DNA Methylation in the COL1A2 Promoter by Anacardic Acid Prevents UV-Induced Decrease of Type I Procollagen Expression.
[So] Source:J Invest Dermatol;137(6):1343-1352, 2017 Jun.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UV radiation decreases type I procollagen production mainly by inhibiting the transforming growth factor-ß/Smad signaling pathway. Because further epigenetic regulatory mechanisms are unclear, we investigated the roles of DNA methylation and histone acetylation in UV-induced regulation of COL1A2 transcription in human dermal fibroblasts. Anacardic acid, a p300 histone acetyltransferase inhibitor, rescued the UV-induced decrease of type I procollagen expression in human dermal fibroblasts. Although UV irradiation induced global histone acetylation, it reduced the local recruitment of histone H3 acetylation as well as p300, and Smad2/3 to the p300 binding site (-1406/-1393), in the COL1A2 promoter as shown by chromatin immunoprecipitation. This effect was reversed by anacardic acid treatment. In contrast, pyrosequencing analysis showed that UV irradiation induced DNA methylation in the same region of the COL1A2 promoter, which was reversed by anacardic acid and a DNA methyltransferase inhibitor (5-AZA-2'-deoxycytidine). Inhibition of UV-induced DNA methylation led to an increase of UV-induced histone acetylation in the COL1A2 promoter and increased the recruitment of transcription factors, leading to up-regulation of type I collagen after UV irradiation. Collectively, our findings indicate that the epigenetic crosstalk between DNA methylation and histone acetylation plays a crucial role in COL1A2 transcription induced by UV irradiation.
[Mh] Termos MeSH primário: Ácidos Anacárdicos/farmacologia
Colágeno Tipo I/genética
Metilação de DNA/efeitos da radiação
Raios Ultravioleta/efeitos adversos
[Mh] Termos MeSH secundário: Acetilação
Células Cultivadas
Imunoprecipitação da Cromatina
Colágeno Tipo I/efeitos da radiação
Proteínas de Ligação a DNA/metabolismo
Proteína p300 Associada a E1A/metabolismo
Fibroblastos/citologia
Fibroblastos/efeitos da radiação
Histonas/metabolismo
Seres Humanos
Regiões Promotoras Genéticas
Ativação Transcricional/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anacardic Acids); 0 (COL1A2 protein, human); 0 (Collagen Type I); 0 (DNA-Binding Proteins); 0 (Histones); EC 2.3.1.48 (E1A-Associated p300 Protein); EC 2.3.1.48 (EP300 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170227
[St] Status:MEDLINE


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[PMID]:28194469
[Au] Autor:Peng C; Luo X; Li S; Sun H
[Ad] Endereço:Department of Pediatrics, Affiliated Hospital of Zunyi Medical College, Guizhou, China.
[Ti] Título:Phenylephrine-induced cardiac hypertrophy is attenuated by a histone acetylase inhibitor anacardic acid in mice.
[So] Source:Mol Biosyst;13(4):714-724, 2017 Mar 28.
[Is] ISSN:1742-2051
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cardiac hypertrophy is a complex process involving highly coordinated but tight regulation of multiple elements, such as in epigenetics, which make an important contribution to myocardium remodeling and cardiac hypertrophy. Epigenetic regulations, particularly histone acetylation, have been implicated in cardiac hypertrophy, however, the exact mechanism is still largely unknown. In the present study, we explored the potential attenuating effects of Chinese herbal extract anacardic acid on phenylephrine-induced cardiac hypertrophy and the underlying mechanism. The mouse cardiac hypertrophy model was established and the hearts were collected from C57BL/6 mice for further analyses. The data showed that anacardic acid modulated the cardiac genes expression and attenuated the phenylephrine-induced cardiac hypertrophy via the suppression of histone acetylases activity and downstream cardiac genes. In addition, anacardic acid abrogated histone and MEF2A acetylation and DNA-binding activity by blocking p300-HAT and PCAF-HAT activities. In addition, anacardic acid normalized the cardiac hypertrophy-related genes expressions (ANP, BNP, cTnT, cTnI, ß-MHC, and Cx43) induced by phenylephrine at the level of transcription and translation. In addition, anacardic acid did not affect the blood routine index, hepatic function, renal function, and myocardial enzymes. Therefore, anacardic acid may prove to be a candidate drug to cure hypertrophic cardiomyopathy.
[Mh] Termos MeSH primário: Ácidos Anacárdicos/farmacologia
Cardiomegalia/metabolismo
Histona Acetiltransferases/antagonistas & inibidores
[Mh] Termos MeSH secundário: Acetilação
Animais
Cardiomegalia/induzido quimicamente
Cardiomegalia/diagnóstico
Cardiomegalia/tratamento farmacológico
Modelos Animais de Doenças
Feminino
Perfilação da Expressão Gênica
Regulação da Expressão Gênica/efeitos dos fármacos
Testes de Função Cardíaca
Histona Acetiltransferases/metabolismo
Histonas/metabolismo
Fatores de Transcrição MEF2/genética
Masculino
Camundongos
Miocárdio/metabolismo
Miocárdio/patologia
Fenilefrina/efeitos adversos
Ligação Proteica
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anacardic Acids); 0 (Histones); 0 (MEF2 Transcription Factors); 18654-18-7 (anacardic acid); 1WS297W6MV (Phenylephrine); EC 2.3.1.48 (Histone Acetyltransferases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE
[do] DOI:10.1039/c6mb00692b


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[PMID]:28108335
[Au] Autor:Melo FR; Wallerman O; Paivandy A; Calounova G; Gustafson AM; Sabari BR; Zabucchi G; Allis CD; Pejler G
[Ad] Endereço:Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden. Electronic address: Fabio.Melo@imbim.uu.se.
[Ti] Título:Tryptase-catalyzed core histone truncation: A novel epigenetic regulatory mechanism in mast cells.
[So] Source:J Allergy Clin Immunol;140(2):474-485, 2017 Aug.
[Is] ISSN:1097-6825
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mast cells are key effector cells in allergic reactions. When activated to degranulate, they release a plethora of bioactive compounds from their secretory granules, including mast cell-restricted proteases such as tryptase. In a previous study, we showed that tryptase, in addition to its intragranular location, can be found within the nuclei of mast cells where it truncates core histones at their N-terminal ends. OBJECTIVE: Considering that the N-terminal portions of the core histones constitute sites for posttranslational modifications of major epigenetic impact, we evaluated whether histone truncation by tryptase could have an impact on epigenetic events in mast cells. METHODS: Mast cells were cultured from wild-type and tryptase null mice, followed by an assessment of their profile of epigenetic histone modifications and their phenotypic characteristics. RESULTS: We show that tryptase truncates nucleosomal histone 3 and histone 2B (H2B) and that its absence results in accumulation of the epigenetic mark, lysine 5-acetylated H2B. Intriguingly, the accumulation of lysine 5-acetylated H2B was cell age-dependent and was associated with a profound upregulation of markers of non-mast cell lineages, loss of proliferative control, chromatin remodeling as well as extensive morphological alterations. CONCLUSIONS: These findings introduce tryptase-catalyzed histone clipping as a novel epigenetic regulatory mechanism, which in the mast cell context may be crucial for maintaining cellular identity.
[Mh] Termos MeSH primário: Histonas/metabolismo
Mastócitos/metabolismo
Triptases/metabolismo
[Mh] Termos MeSH secundário: Acetilação
Ácidos Anacárdicos/farmacologia
Animais
Catepsina G/genética
Células Cultivadas
Epigênese Genética
Regulação da Expressão Gênica
Inibidores de Histona Desacetilases/farmacologia
Lisina/metabolismo
Mastócitos/efeitos dos fármacos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteoglicanas/genética
Triptases/genética
Proteínas de Transporte Vesicular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anacardic Acids); 0 (Histone Deacetylase Inhibitors); 0 (Histones); 0 (Proteoglycans); 0 (Vesicular Transport Proteins); 0 (serglycin); 18654-18-7 (anacardic acid); EC 3.4.21.20 (Cathepsin G); EC 3.4.21.20 (Ctsg protein, mouse); EC 3.4.21.59 (Tryptases); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170122
[St] Status:MEDLINE


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[PMID]:27916539
[Au] Autor:Bogachek MV; Park JM; De Andrade JP; Lorenzen AW; Kulak MV; White JR; Gu VW; Wu VT; Weigel RJ
[Ad] Endereço:Department of Surgery, University of Iowa, 200 Hawkins Drive, 1516 JCP, Iowa City, IA 52242, USA.
[Ti] Título:Inhibiting the SUMO Pathway Represses the Cancer Stem Cell Population in Breast and Colorectal Carcinomas.
[So] Source:Stem Cell Reports;7(6):1140-1151, 2016 Dec 13.
[Is] ISSN:2213-6711
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many solid cancers have an expanded CD44 /CD24 cancer stem cell (CSC) population, which are relatively chemoresistant and drive recurrence and metastasis. Achieving a more durable response requires the development of therapies that specifically target CSCs. Recent evidence indicated that inhibiting the SUMO pathway repressed tumor growth and invasiveness, although the mechanism has yet to be clarified. Here, we demonstrate that inhibition of the SUMO pathway repressed MMP14 and CD44 with a concomitant reduction in cell invasiveness and functional loss of CSCs in basal breast cancer. Similar effects were demonstrated with a panel of E1 and E3 SUMO inhibitors. Identical results were obtained in a colorectal cancer cell line and primary colon cancer cells. In both breast and colon cancer, SUMO-unconjugated TFAP2A mediated the effects of SUMO inhibition. These data support the development of SUMO inhibitors as an approach to specifically target the CSC population in breast and colorectal cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Neoplasias Colorretais/patologia
Células-Tronco Neoplásicas/metabolismo
Células-Tronco Neoplásicas/patologia
Transdução de Sinais
Proteínas Modificadoras Pequenas Relacionadas à Ubiquitina/metabolismo
[Mh] Termos MeSH secundário: Ácidos Anacárdicos/química
Ácidos Anacárdicos/farmacologia
Neoplasias da Mama/metabolismo
Carcinogênese/efeitos dos fármacos
Carcinogênese/metabolismo
Carcinogênese/patologia
Linhagem Celular Tumoral
Neoplasias Colorretais/metabolismo
Feminino
Técnicas de Silenciamento de Genes
Seres Humanos
Receptores de Hialuronatos/metabolismo
Metaloproteinase 14 da Matriz/metabolismo
Invasividade Neoplásica
Células-Tronco Neoplásicas/efeitos dos fármacos
Fenótipo
Transdução de Sinais/efeitos dos fármacos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anacardic Acids); 0 (CD44 protein, human); 0 (Hyaluronan Receptors); 0 (Small Ubiquitin-Related Modifier Proteins); 18654-18-7 (anacardic acid); EC 3.4.24.80 (Matrix Metalloproteinase 14)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161206
[St] Status:MEDLINE


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[PMID]:27737732
[Au] Autor:Nambiar J; Bose C; Venugopal M; Banerji A; Patel TB; Kumar GB; Nair BG
[Ad] Endereço:Amrita School of Biotechnology, Amrita Vishwa Vidyapeetham, Amritapuri, Clappana P.O., Kollam 690525, Kerala, India.
[Ti] Título:Anacardic acid inhibits gelatinases through the regulation of Spry2, MMP-14, EMMPRIN and RECK.
[So] Source:Exp Cell Res;349(1):139-151, 2016 Nov 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Earlier studies from our laboratory have identified Anacardic acid (AA) as a potent inhibitor of gelatinases (MMP-2 and 9), which are over-expressed in a wide variety of cancers (Omanakuttan et al., 2012). Disruption of the finely tuned matrix metalloproteinase (MMP) activator/inhibitor balance plays a decisive role in determining the fate of the cell. The present study demonstrates for the first time, that in addition to regulating the expression as well as activity of gelatinases, AA also inhibits the expression of its endogenous activators like MMP-14 and Extracellular Matrix MetalloProteinase Inducer (EMMPRIN) and induces the expression of its endogenous inhibitor, REversion-inducing Cysteine-rich protein with Kazal motifs (RECK). In addition to modulating gelatinases, AA also inhibits the expression of various components of the Epidermal Growth Factor (EGF) pathway like EGF, Protein Kinase B (Akt) and Mitogen-activated protein kinases (MAPK). Furthermore, AA also activates the expression of Sprouty 2 (Spry2), a negative regulator of EGF pathway, and silencing Spry2 results in up-regulation of expression of gelatinases as well as MMP-14. The present study thus elucidates a novel mechanism of action of AA and provides a strong basis for utilizing this molecule as a template for cancer therapeutics.
[Mh] Termos MeSH primário: Ácidos Anacárdicos/farmacologia
Basigina/metabolismo
Proteínas Ligadas por GPI/metabolismo
Gelatinases/antagonistas & inibidores
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Metaloproteinase 14 da Matriz/metabolismo
Proteínas de Membrana/metabolismo
[Mh] Termos MeSH secundário: Adesão Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Fator de Crescimento Epidérmico/metabolismo
Gelatinases/metabolismo
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/metabolismo
Inibidores de Metaloproteinases de Matriz/farmacologia
Modelos Biológicos
Invasividade Neoplásica
Transdução de Sinais/efeitos dos fármacos
Inibidor Tecidual de Metaloproteinase-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anacardic Acids); 0 (GPI-Linked Proteins); 0 (Intracellular Signaling Peptides and Proteins); 0 (Matrix Metalloproteinase Inhibitors); 0 (Membrane Proteins); 0 (RECK protein, human); 0 (SPRY2 protein, human); 127497-59-0 (Tissue Inhibitor of Metalloproteinase-2); 136894-56-9 (Basigin); 18654-18-7 (anacardic acid); 62229-50-9 (Epidermal Growth Factor); EC 3.4.24.- (Gelatinases); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.80 (MMP14 protein, human); EC 3.4.24.80 (Matrix Metalloproteinase 14)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161015
[St] Status:MEDLINE


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[PMID]:27430733
[Au] Autor:Dong X; Liao Y; Liu N; Hua X; Cai J; Liu J; Huang H
[Ad] Endereço:Protein Modification and Degradation Laboratory, Department of Pathophysiology, Guangzhou Medical University, Guangzhou, Guangdong 510182, P.R. China.
[Ti] Título:Combined therapeutic effects of bortezomib and anacardic acid on multiple myeloma cells via activation of the endoplasmic reticulum stress response.
[So] Source:Mol Med Rep;14(3):2679-84, 2016 Sep.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Bortezomib (Bor), a proteasome inhibitor, has marked therapeutic effects in multiple myeloma (MM), and its synergistic effects with other anticancer agents have been widely investigated. In the present study, endoplasmic reticulum (ER) stress was the target of the treatment strategy; anacardic acid (AA) and Bor induce ER stress, resulting in apoptosis of multiple myeloma cells. AA/Bor combination therapy exhibited overt cytotoxicity in MM cells, by synergistically reducing cell growth and promoting cell death. Notably, expression levels of the stress­associated molecules binding protein, phosphorylated eukaryotic initiation factor 2α, activating transcription factor 4 (ATF4) and CCAAT­enhancer binding protein homologous protein (CHOP) were increased following treatment. AA/Bor combination therapy­induced U266 cell cytotoxicity was partially reversed by ATF4 gene silencing and slightly enhanced by CHOP knockdown. The results of the present study suggest that AA/Bor combination may be a potential therapeutic strategy for MM treatment.
[Mh] Termos MeSH primário: Ácidos Anacárdicos/farmacologia
Bortezomib/farmacologia
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Mieloma Múltiplo/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Caspases/metabolismo
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Sinergismo Farmacológico
Estresse do Retículo Endoplasmático/genética
Seres Humanos
Mieloma Múltiplo/genética
Fator de Transcrição CHOP/genética
Fator de Transcrição CHOP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anacardic Acids); 0 (DDIT3 protein, human); 147336-12-7 (Transcription Factor CHOP); 69G8BD63PP (Bortezomib); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170406
[Lr] Data última revisão:
170406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160720
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2016.5533


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[PMID]:27226531
[Au] Autor:Hollands A; Corriden R; Gysler G; Dahesh S; Olson J; Raza Ali S; Kunkel MT; Lin AE; Forli S; Newton AC; Kumar GB; Nair BG; Perry JJ; Nizet V
[Ad] Endereço:From the Departments of Pediatrics and.
[Ti] Título:Natural Product Anacardic Acid from Cashew Nut Shells Stimulates Neutrophil Extracellular Trap Production and Bactericidal Activity.
[So] Source:J Biol Chem;291(27):13964-73, 2016 Jul 01.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Emerging antibiotic resistance among pathogenic bacteria is an issue of great clinical importance, and new approaches to therapy are urgently needed. Anacardic acid, the primary active component of cashew nut shell extract, is a natural product used in the treatment of a variety of medical conditions, including infectious abscesses. Here, we investigate the effects of this natural product on the function of human neutrophils. We find that anacardic acid stimulates the production of reactive oxygen species and neutrophil extracellular traps, two mechanisms utilized by neutrophils to kill invading bacteria. Molecular modeling and pharmacological inhibitor studies suggest anacardic acid stimulation of neutrophils occurs in a PI3K-dependent manner through activation of surface-expressed G protein-coupled sphingosine-1-phosphate receptors. Neutrophil extracellular traps produced in response to anacardic acid are bactericidal and complement select direct antimicrobial activities of the compound.
[Mh] Termos MeSH primário: Ácidos Anacárdicos/farmacologia
Anacardium/química
Antibacterianos/farmacologia
Armadilhas Extracelulares/metabolismo
Neutrófilos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Seres Humanos
Lisofosfolipídeos/metabolismo
Explosão Respiratória
Esfingosina/análogos & derivados
Esfingosina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Anacardic Acids); 0 (Anti-Bacterial Agents); 0 (Lysophospholipids); 18654-18-7 (anacardic acid); 26993-30-6 (sphingosine 1-phosphate); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160527
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M115.695866



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