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[PMID]:29267503
[Au] Autor:Wang ZK; Yang L; Wu LL; Mao H; Zhou YH; Zhang PF; Dai GH
[Ad] Endereço:The Second Department of Medical Oncology, Chinese People's Liberation Army General Hospital, Beijing, China.
[Ti] Título:Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy.
[So] Source:Braz J Med Biol Res;51(2):e6793, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Colon cancer is one of the most common digestive tumors. The present study aimed to explore the functional role, as well as the underlying mechanism of long non-coding RNA LINC00261 in colon cancer. Expression of LINC00261 was analyzed in colon cancer cell lines and human normal cell lines. Acquired resistance cell lines were then built and the acquired resistance efficiency was detected by evaluating cell viability. Thereafter, the effects of LINC00261 overexpression on cisplatin-resistant colon cancer cells were measured, as well as cell apoptosis, viability, migration, and invasion. Subsequently, we investigated the interaction of LINC00261 and ß-catenin. The results showed that the LINC00261 gene was down-regulated in colon cancer cell lines and tissues, and in cisplatin-resistant cells. LINC00261 overexpression might relieve cisplatin resistance of colon cancer cells via promoting cell apoptosis, and inhibiting cell viability, migration, and invasion. Moreover, LINC00261 might down-regulate nuclear ß-catenin through restraining ß-catenin from cytoplasm into nuclei or it could also promote ß-catenin degradation and inhibit activation of Wnt pathway. Finally, LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Cisplatino/farmacologia
Neoplasias do Colo/tratamento farmacológico
Neoplasias do Colo/genética
Neoplasias do Colo/patologia
RNA Longo não Codificante/fisiologia
[Mh] Termos MeSH secundário: Análise de Variância
Apoptose/efeitos dos fármacos
Apoptose/fisiologia
Proteínas Reguladoras de Apoptose/efeitos dos fármacos
Proteínas Reguladoras de Apoptose/fisiologia
Western Blotting
Ensaios de Migração Celular
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/fisiologia
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/fisiologia
Células HCT116
Células HT29
Seres Humanos
RNA Longo não Codificante/análise
RNA Longo não Codificante/efeitos dos fármacos
RNA Longo não Codificante/genética
Reprodutibilidade dos Testes
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/fisiologia
Sais de Tetrazólio
Tiazóis
beta Catenina/efeitos dos fármacos
beta Catenina/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Apoptosis Regulatory Proteins); 0 (RNA, Long Noncoding); 0 (Tetrazolium Salts); 0 (Thiazoles); 0 (beta Catenin); 0 (long non-coding RNA 00261, human); EUY85H477I (thiazolyl blue); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29205962
[Au] Autor:Lin JY; Mao X; Wu HJ; Xue AM
[Ad] Endereço:Department of Forensic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
[Ti] Título:[Genes Expression in the Early Stage of Acute Renal Ischemia-reperfusion Injury in Rats].
[So] Source:Fa Yi Xue Za Zhi;32(6):401-405, 2016 Dec.
[Is] ISSN:1004-5619
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVES: To study the differential genes expression in the early stage of acute renal ischemia-reperfusion injury and explore potential molecular mechanisms. METHODS: The ischemia-reperfusion model was made via clamping renal artery of rat. The microarray detection and bioinformatics analyzing of the genes expression were performed. Differentially expressed genes were screened and related cellular activities and signaling pathways were analyzed in early stage of acute kidney injury. Meanwhile, molecules closely relative to acute kidney injury were explored by establishing a biological network of the differentially expressed genes, and the results were verified by real-time PCR. RESULTS: A total of 151 genes showed differential expression in this study, including 132 up-regulated and 19 down-regulated genes. Cell proliferation, cytokines mediated signaling transduction and immune responses were greatly enriched by GO and KEGG analysis. The results of real-time PCR showed that compared with control groups, three selected genes ( , and ) which related to the acute kidney injury had an obvious differential expression in the early stage of disease. The multiple of increase was essentially the same as the multiple detected by microarray. CONCLUSIONS: This study shows differential gene expression profile, related biological processes and signaling pathways involved in the early stage of acute kidney injury. , and may play a role in the pathogenesis of acute kidney injury.
[Mh] Termos MeSH primário: Lesão Renal Aguda/genética
Traumatismo por Reperfusão/genética
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Anexina A1/genética
Proteínas Reguladoras de Apoptose/genética
Expressão Gênica
Rim/patologia
Fator 6 Semelhante a Kruppel/genética
Ratos
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A1); 0 (Apoptosis Regulatory Proteins); 0 (Klf6 protein, rat); 0 (Kruppel-Like Factor 6); 0 (Phlda1 protein, rat)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.3969/j.issn.1004-5619.2016.06.001


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[PMID]:28460441
[Au] Autor:Arora J; Sauer SJ; Tarpley M; Vermeulen P; Rypens C; Van Laere S; Williams KP; Devi GR; Dewhirst MW
[Ad] Endereço:Duke Cancer Institute, Duke University, Durham, NC, USA.
[Ti] Título:Inflammatory breast cancer tumor emboli express high levels of anti-apoptotic proteins: use of a quantitative high content and high-throughput 3D IBC spheroid assay to identify targeting strategies.
[So] Source:Oncotarget;8(16):25848-25863, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammatory breast cancer (IBC) is one of the most lethal breast cancer variants; with existing therapy, 5-yr survival rate is only 35%. Current barriers to successful treatment of IBC include frequent infiltration and the presence of tumor cell clusters, termed tumor emboli, within the breast parenchyma and lymphatics. Prior studies have identified the role of anti-apoptotic signaling, in particular hyperactivation of NFκB and its target genes, in IBC pathobiology and therapeutic resistance. The objectives of this study were to: (1) determine if IBC tumor emboli express anti-apoptotic proteins and (2) develop a high content, multiparametric assay to assess the morphology of the IBC 3D spheroids and to optimize a high throughput format to screen for compounds that can inhibit the formation of the IBC tumor clusters/embolic structures. Immunohistochemical analysis of IBC patient tumor samples with documented tumor emboli revealed high NFκB (p65) staining along with expression of XIAP, a potent anti-apoptotic protein known to interact with NFκB signaling in enhancing survival of malignant cells. Subsequently, the high content assay developed allowed for simultaneous imaging and morphometric analysis, including count and viability of spheroids derived from SUM149, rSUM149 and SUM190 cells and its application to evaluate XIAP and NFκB inhibitory agents. We demonstrate the efficacy of the off-patent drug disulfiram when chelated with copper, which we had previously reported to inhibit NFκB signaling, was highly effective in disrupting both IBC spheroids and emboli grown in vitro. Taken together, these results identify a high-throughput approach to target tumor spheroid formation for drug discovery. Finally, disulfiram is a safe and approved drug for management of alcohol abuse, warranting its evaluation for repurposing in IBC therapy.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/genética
Neoplasias Inflamatórias Mamárias/genética
Neoplasias Inflamatórias Mamárias/patologia
Células Neoplásicas Circulantes/metabolismo
[Mh] Termos MeSH secundário: Proteínas Reguladoras de Apoptose/metabolismo
Biomarcadores Tumorais
Técnicas de Cultura de Células
Sobrevivência Celular/genética
Cobre/farmacologia
Dissulfiram/farmacologia
Feminino
Expressão Gênica
Ensaios de Triagem em Larga Escala
Seres Humanos
Neoplasias Inflamatórias Mamárias/metabolismo
Mitocôndrias/metabolismo
NF-kappa B/genética
NF-kappa B/metabolismo
Esferoides Celulares
Células Tumorais Cultivadas
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/genética
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (Biomarkers, Tumor); 0 (NF-kappa B); 0 (X-Linked Inhibitor of Apoptosis Protein); 0 (XIAP protein, human); 789U1901C5 (Copper); TR3MLJ1UAI (Disulfiram)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15667


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[PMID]:28464919
[Au] Autor:Toth C; Funke S; Nitsche V; Liverts A; Zlachevska V; Gasis M; Wiek C; Hanenberg H; Mahotka C; Schirmacher P; Heikaus S
[Ad] Endereço:Institute of Pathology, Heinrich Heine University Hospital, Medical Faculty, Moorenstrasse 5, 40225, Düsseldorf, Germany. csaba.toth@med.uni-heidelberg.de.
[Ti] Título:The role of apoptosis repressor with a CARD domain (ARC) in the therapeutic resistance of renal cell carcinoma (RCC): the crucial role of ARC in the inhibition of extrinsic and intrinsic apoptotic signalling.
[So] Source:Cell Commun Signal;15(1):16, 2017 May 02.
[Is] ISSN:1478-811X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Renal cell carcinomas (RCCs) display broad resistance against conventional radio- and chemotherapies, which is due at least in part to impairments in both extrinsic and intrinsic apoptotic pathways. One important anti-apoptotic factor that is strongly overexpressed in RCCs and known to inhibit both apoptotic pathways is ARC (apoptosis repressor with a CARD domain). METHODS: Expression and subcellular distribution of ARC in RCC tissue samples and RCC cell lines were determined by immunohistochemistry and fluorescent immunohistochemistry, respectively. Extrinsic and intrinsic apoptosis signalling were induced by TRAIL (TNF-related apoptosis-inducing ligand), ABT-263 or topotecan. ARC knock-down was performed in clearCa-12 cells using lentiviral transduction of pGIPZ. shRNAmir constructs. Extrinsic respectively intrinsic apoptosis were induced by TRAIL (TNF-related apoptosis-inducing ligand), ABT263 or topotecan. Potential synergistic effects were tested by pre-treatment with topotecan and subsequent treatment with ABT263. Activation of different caspases and mitochondrial depolarisation (JC-1 staining) were analysed by flow cytometry. Protein expression of Bcl-2 family members and ARC in RCC cell lines was measured by Western blotting. Statistical analysis was performed by Student's t-test. RESULTS: Regarding the extrinsic pathway, ARC knockdown strongly enhanced TRAIL-induced apoptosis by increasing the activation level of caspase-8. Regarding the intrinsic pathway, ARC, which was only weakly expressed in the nuclei of RCCs in vivo, exerted its anti-apoptotic effect by impairing mitochondrial activation rather than inhibiting p53. Topotecan- and ABT-263-induced apoptosis was strongly enhanced following ARC knockdown in RCC cell lines. In addition, topotecan pre-treatment enhanced ABT-263-induced apoptosis and this effect was amplified in ARC-knockdown cells. CONCLUSION: Taken together, our results are the first to demonstrate the importance of ARC protein in the inhibition of both the extrinsic and intrinsic pathways of apoptosis in RCCs. In this context, ARC cooperates with anti-apoptotic Bcl-2 family members to exert its strong anti-apoptotic effects and is therefore an important factor not only in the therapeutic resistance but also in future therapy strategies (i.e., Bcl-2 inhibitors) in RCC. In sum, targeting of ARC may enhance the therapeutic response in combination therapy protocols.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/metabolismo
Apoptose/efeitos dos fármacos
Carcinoma de Células Renais/patologia
Resistência a Medicamentos Antineoplásicos
Neoplasias Renais/patologia
Proteínas Musculares/metabolismo
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular/efeitos dos fármacos
Compostos de Anilina/farmacologia
Proteínas Reguladoras de Apoptose/deficiência
Proteínas Reguladoras de Apoptose/genética
Linhagem Celular Tumoral
Núcleo Celular/efeitos dos fármacos
Núcleo Celular/metabolismo
Citoplasma/efeitos dos fármacos
Citoplasma/metabolismo
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Seres Humanos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/patologia
Terapia de Alvo Molecular
Proteínas Musculares/deficiência
Proteínas Musculares/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Sulfonamidas/farmacologia
Topotecan/farmacologia
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Apoptosis Regulatory Proteins); 0 (Muscle Proteins); 0 (NOL3 protein, human); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Sulfonamides); 0 (Tumor Suppressor Protein p53); 7M7YKX2N15 (Topotecan); XKJ5VVK2WD (navitoclax)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12964-017-0170-5


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[PMID]:29374163
[Au] Autor:Márquez-Jurado S; Díaz-Colunga J; das Neves RP; Martinez-Lorente A; Almazán F; Guantes R; Iborra FJ
[Ad] Endereço:Department of Molecular and Cell Biology, Centro Nacional de Biotecnología (CNB-CSIC), Campus de Cantoblanco, 28049, Madrid, Spain.
[Ti] Título:Mitochondrial levels determine variability in cell death by modulating apoptotic gene expression.
[So] Source:Nat Commun;9(1):389, 2018 01 26.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fractional killing is the main cause of tumour resistance to chemotherapy. This phenomenon is observed even in genetically identical cancer cells in homogeneous microenvironments. To understand this variable resistance, here we investigate the individual responses to TRAIL in a clonal population of HeLa cells using live-cell microscopy and computational modelling. We show that the cellular mitochondrial content determines the apoptotic fate and modulates the time to death, cells with higher mitochondrial content are more prone to die. We find that all apoptotic protein levels are modulated by the mitochondrial content. Modelling the apoptotic network, we demonstrate that these correlations, and especially the differential control of anti- and pro-apoptotic protein pairs, confer mitochondria a powerful discriminatory capacity of apoptotic fate. We find a similar correlation between the mitochondria and apoptotic proteins in colon cancer biopsies. Our results reveal a different role of mitochondria in apoptosis as the global regulator of apoptotic protein expression.
[Mh] Termos MeSH primário: Apoptose/genética
Expressão Gênica/genética
Mitocôndrias/genética
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Algoritmos
Apoptose/efeitos dos fármacos
Proteínas Reguladoras de Apoptose/genética
Proteínas Reguladoras de Apoptose/metabolismo
Morte Celular/genética
Expressão Gênica/efeitos dos fármacos
Células HeLa
Seres Humanos
Mitocôndrias/metabolismo
Modelos Genéticos
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (Reactive Oxygen Species); 0 (TNF-Related Apoptosis-Inducing Ligand)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180128
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02787-4


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[PMID]:29339102
[Au] Autor:Khafaga AF; El-Sayed YS
[Ad] Endereço:Department of Pathology, Faculty of Veterinary Medicine, Alexandria University, Edfina 22758, Egypt. Electronic address: asmaa.khafaga@alexu.edu.eg.
[Ti] Título:Spirulina ameliorates methotrexate hepatotoxicity via antioxidant, immune stimulation, and proinflammatory cytokines and apoptotic proteins modulation.
[So] Source:Life Sci;196:9-17, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Methotrexate (MTX) is an efficient cytotoxic drug used against various carcinogenic, inflammatory and autoimmune diseases; however, the hepatotoxicity of MTX limits its use. Therefore, the present study aimed to evaluate the potential hepatoprotective and immune-stimulant effect of Spirulina platensis (SP) against MTX acute toxicity. MAIN METHODS: Thirty-two male Wistar rats were randomly allocated into the following four groups (n = 8): control, SP (500 mg/kg bwt, oral gavage daily for 21 days), MTX (20 mg/kg bwt, single ip injection), and MTX+SP. Hepatic and splenic histoarchitecture, leukocyte counts and serum immunoglobulins were evaluated. Hepatic oxidant/antioxidant status, proinflammatory cytokines (tumor necrosis factor-α, and interleukin 6), and pro-apoptotic proteins (caspase 3 and Bax) immunoexpression were assessed. KEY FINDINGS: MTX induced extensive hepatic necrosis and vacuolation, and sever lymphoid depletion in splenic white pulp with increased levels of serum transaminases, lactate dehydrogenase, and hepatic malondialdehyde, tumor necrosis factor-α and interleukin 6; and number of caspase 3- and Bax-positive hepatocytes. A significant decrease in leukocyte counts, serum immunoglobulins (IgA, IgM and IgG) level, and hepatic antioxidant enzymes (GSH, GPx, SOD, and CAT) was also detected. Pretreatment with SP resulted in significant improvements in hepatic and splenic histologic architecture, as well as restoring liver enzymes and reduction of lipid peroxidation product, proinflammatory cytokines, and caspase 3 and Bax immunoexpression. Additionally, a significant increase in antioxidant enzymes, serum immunoglobulins, and total leukocyte counts was demonstrated. SIGNIFICANCE: SP possesses promising antioxidant, anti-inflammatory, anti-apoptotic and immune stimulatory properties against MTX-induced hepatotoxicity and immunosuppression.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/farmacologia
Antimetabólitos/toxicidade
Antioxidantes/farmacologia
Proteínas Reguladoras de Apoptose/antagonistas & inibidores
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Citocinas/antagonistas & inibidores
Metotrexato/antagonistas & inibidores
Metotrexato/toxicidade
Extratos Vegetais/farmacologia
Spirulina/química
[Mh] Termos MeSH secundário: Animais
Contagem de Leucócitos
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Necrose
Ratos
Ratos Wistar
Baço/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Antimetabolites); 0 (Antioxidants); 0 (Apoptosis Regulatory Proteins); 0 (Cytokines); 0 (Plant Extracts); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


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[PMID]:29305708
[Au] Autor:Sikaria D; Tu YN; Fisler DA; Mauro JA; Blanck G
[Ad] Endereço:Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, USA.
[Ti] Título:Identification of specific feed-forward apoptosis mechanisms and associated higher survival rates for low grade glioma and lung squamous cell carcinoma.
[So] Source:J Cancer Res Clin Oncol;144(3):459-468, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The mechanisms of cell proliferation due to the overexpression of certain transcription factors (TFs) have been well documented in the cancer setting. However, many of these same TFs have pro-apoptotic effects, particularly when expressed or activated at high levels, a process referred to as feed-forward apoptosis (FFA). To determine whether cancers could be stratified on the basis of specific FFA signatures, RNASeq data representing samples from the cancer genome atlas were analyzed, revealing that high expression of the pro-proliferative TFs, MYC and YY1, is associated with a favorable outcome in low-grade glioma (LGG) and lung squamous cell carcinoma (LUSC), respectively. Analysis of the RNASeq data also led to the identification of specific apoptosis-effector genes whose expression levels correlate with increased survival rates, for both LGG and LUSC. Although FFA has been demonstrated as a general effect in cancer, in this report, for the first time, results identify specific TFs and their responsive effector genes that distinguish subsets of cancer samples undergoing more or less of a FFA process in a way that is associated with distinct patient survival rates.
[Mh] Termos MeSH primário: Apoptose/fisiologia
Carcinoma de Células Escamosas/mortalidade
Carcinoma de Células Escamosas/patologia
Glioma/mortalidade
Glioma/patologia
Neoplasias Pulmonares/mortalidade
Neoplasias Pulmonares/patologia
[Mh] Termos MeSH secundário: Apoptose/genética
Proteínas Reguladoras de Apoptose/genética
Carcinoma de Células Escamosas/genética
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Glioma/genética
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Neoplasias Pulmonares/genética
Gradação de Tumores
Transdução de Sinais/genética
Taxa de Sobrevida
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (Transcription Factors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2569-1


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[PMID]:29372685
[Au] Autor:Fialkova V; Vidomanova E; Balharek T; Marcinek J; Kudela E; Hanysova S; Visnovsky J; Dobrota D; Hatok J
[Ad] Endereço:Department of Medical Biochemistry, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovakia. hatok@jfmed.uniba.sk.
[Ti] Título:DNA methylation as mechanism of apoptotic resistance development in endometrial cancer patients.
[So] Source:Gen Physiol Biophys;36(5):521-529, 2017 Dec.
[Is] ISSN:0231-5882
[Cp] País de publicação:Slovakia
[La] Idioma:eng
[Ab] Resumo:DNA methylation is a significant epigenetic modification which plays a key role in regulation of gene expression and influences functional changes in endometrial tissue. Aberrant DNA methylation changes result in deregulation of important apoptotic proteins during endometrial carcinogenesis and apoptosis resistance development. Evading apoptosis is still a major problem in the successful treatment of endometrial cancer patients. The aim of our study was to examine the promoter DNA methylation changes in 22 apoptosis-associated genes in endometrioid endometrial cancer patients, precancerous lesions and healthy tissue from various normal menstrual cycle phases using a unique pre-designed methylation platform. We observed as the first a significant difference in promoter DNA methylation status in genes: BCL2L11 (p < 0.001), CIDEB (p < 0.03) and GADD45A (p < 0.05) during endometrial carcinogenesis and BIK gene (p < 0.03) in different phases of normal menstrual cycle. The results of our study indicate that deregulation of mitochondrial apoptotic pathway can considerably contributes to the apoptosis resistance development and may be helpful in identifying of new potent biomarkers in endometrial cancer.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/genética
Apoptose/genética
Metilação de DNA/genética
DNA de Neoplasias/genética
Neoplasias do Endométrio/genética
Epigênese Genética/genética
Lesões Pré-Cancerosas/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinogênese/genética
Feminino
Predisposição Genética para Doença/genética
Seres Humanos
Meia-Idade
Polimorfismo de Nucleotídeo Único/genética
Eslováquia
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (DNA, Neoplasm)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.4149/gpb_2017032


  9 / 14602 MEDLINE  
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[PMID]:29305260
[Au] Autor:Xu Y; Gao CC; Pan ZG; Zhou CW
[Ad] Endereço:Huai'an First People's Hospital, Nanjing Medical University, No.6, Beijing West Road, Huai'an, 223300, China.
[Ti] Título:Irigenin sensitizes TRAIL-induced apoptosis via enhancing pro-apoptotic molecules in gastric cancer cells.
[So] Source:Biochem Biophys Res Commun;496(3):998-1005, 2018 02 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) holds promising value for cancer therapy due to its capacity to induce apoptosis in cancer cells. Nevertheless, TRAIL therapy is greatly hampered by its resistance. Irigenin (Iri), isoflavonoids, can be isolated from the rhizome of Belamcanda chinensis, and has been shown anti-cancer properties. In this study, we explored if Iri could enhance TRAIL-regulated apoptosis in TRAIL resistant gastric cancer cells. Iri significantly potentiated TRAIL-triggered cytotoxicity. Iri alone and TRAIL alone showed no effective role in apoptosis induction, whereas combined treatment with Iri and TRAIL markedly induced apoptosis in cancer cells, as evidenced by the up-regulation of cleaved Caspase-8/-9/-3 and PARP. Additionally, the sensitization to TRAIL was along with the enhancement of pro-apoptotic proteins, including FAS-associated protein with death domain (FADD), death receptor 5 (DR5) and Bax. And suppressing FADD, DR5 and Bax by si RNA significantly reduced the apoptosis and enhanced the cell viability induced by the co-application of Iri and TRAIL. Moreover, the sensitization to TRAIL was accompanied by the decrease of Cellular-FLICE inhibitory protein (c-FLIP), Bcl-2 and Survivin. Additionally, Iri could sensitize TRAIL to produce reactive oxygen species (ROS). Pre-treatment of N-acetyl-cysteine (NAC), ROS scavenger, attenuated Iri plus TRAIL-induced apoptosis and improved cell viability. Finally, combination of Iri and TRAIL inhibited tumor growth in the xenograft model. Collectively, our present study gave new insights into the effects of Iri on potentiating TRAIL-sensitivity, and suggested that Iri could be a potential candidate for sensitizer of TRAIL-resistant cancer cell treatment.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Proteínas Reguladoras de Apoptose/metabolismo
Apoptose/efeitos dos fármacos
Isoflavonas/administração & dosagem
Neoplasias Gástricas/tratamento farmacológico
Neoplasias Gástricas/metabolismo
Ligante Indutor de Apoptose Relacionado a TNF/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/administração & dosagem
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Sinergismo Farmacológico
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Masculino
Camundongos
Camundongos Nus
Neoplasias Gástricas/patologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Apoptosis Regulatory Proteins); 0 (Isoflavones); 0 (TNF-Related Apoptosis-Inducing Ligand); 6O4NX37350 (irigenin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


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[PMID]:29205955
[Au] Autor:Li B; Weng Q; Liu Z; Shen M; Zhang J; Wu W; Liu H
[Ad] Endereço:College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, People's Republic of China.
[Ti] Título:Selection of antioxidants against ovarian oxidative stress in mouse model.
[So] Source:J Biochem Mol Toxicol;31(12), 2017 Dec.
[Is] ISSN:1099-0461
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxidative stress (OS) plays an important role in the process of ovarian granulosa cell apoptosis and follicular atresia. The aim of this study was to select antioxidant against OS in ovary tissue. Firstly, we chose the six antioxidants and analyzed the reactive oxygen species (ROS) level in the ovary tissue. The results showed that proanthocyanidins, gallic acid, curcumin, and carotene decrease the ROS level compared with control group. We further demonstrated that both proanthocyanidins and gallic acid increase the antioxidant enzymes activity. Moreover, change in the ROS level was not observed in proanthocyanidins and gallic acid group of brain, liver, spleen, and kidney tissues. Finally, we found that proanthocyanidins and gallic acid inhibit pro-apoptotic genes expression in granulosa cells. Taken together, proanthocyanidins and gallic acid may be the most acceptable and optimal antioxidants specifically against ovarian OS and also may be involved in the inhibition of granulosa cells apoptosis in mouse ovary.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Ácido Gálico/farmacologia
Ovário/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Proantocianidinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Proteínas Reguladoras de Apoptose/genética
Proteínas Reguladoras de Apoptose/metabolismo
Avaliação Pré-Clínica de Medicamentos
Feminino
Expressão Gênica/efeitos dos fármacos
Camundongos Endogâmicos ICR
Ovário/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Apoptosis Regulatory Proteins); 0 (Proanthocyanidins); 0 (Reactive Oxygen Species); 18206-61-6 (proanthocyanidin); 632XD903SP (Gallic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1002/jbt.21997



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