Base de dados : MEDLINE
Pesquisa : G04.356.500 [Categoria DeCS]
Referências encontradas : 9309 [refinar]
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  1 / 9309 MEDLINE  
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[PMID]:29394261
[Au] Autor:Patel N; Garikapati KR; Makani VKK; Nair AD; Vangara N; Bhadra U; Pal Bhadra M
[Ad] Endereço:Centre for Chemical Biology, CSIR-Indian Institute of Chemical Technology, Tarnaka, Hyderabad, Telangana State, India.
[Ti] Título:Regulating BMI1 expression via miRNAs promote Mesenchymal to Epithelial Transition (MET) and sensitizes breast cancer cell to chemotherapeutic drug.
[So] Source:PLoS One;13(2):e0190245, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Polycomb group (PcG) proteinB lymphoma Mo-MLV insertion region 1 homolog (BMI1) is a transcriptional repressor that plays an important role in human carcinogenesis. MicroRNAs (miRNAs) are endogenous small non-coding RNAsthat implicate a negative regulation on gene expression. Deregulation of the expression of miRNAs has been implicated in tumorigenesis. Here, we have shown that knock-down ofBMI1increases theexpression of tumor-suppressivemiRNAs. Elevated levels of expression of miR-200a, miR-200b, miR-15a, miR-429, miR-203were observed upon knock-down of BMI1. Up-regulation of these miRNAsleads to down-regulation ofPRC1 group of proteins i.e. BMI1, RING1A, RING1B and Ub-H2A. Interestingly, overexpression of miR-200a, miR-200b and miR-15aalso produced decreased BMI1 and Ub-H2A protein expression in the CD44+ Cancer Stem Cellpopulation of MDAMB-231cells. Also,elevating the levels of BMI1 regulated miRNAspromoted Mesenchymal to Epithelial transition by regulating the expression of N-Cadherin, Vimentin, ß-Catenin, Zeb, Snail thereby resulting in decreased invasion, migration and proliferation. Here, we also report that miR-200a, miR-200b, miR-203 accretes the sensitivity of MDAMB-231 cells to the histone deacetylase inhibitor (HDACi) SAHA and miR-15a sensitized breast cancer cells to the chemotherapeutic drug cisplatin leading to apoptosis. These findings suggest that modulatingspecific miRNAs may serve as a therapeutic approach for the treatment of breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Transição Epitelial-Mesenquimal/genética
Regulação Neoplásica da Expressão Gênica/genética
Complexo Repressor Polycomb 1/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Resistência a Medicamentos Antineoplásicos
Feminino
Seres Humanos
Invasividade Neoplásica
Metástase Neoplásica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (BMI1 protein, human); EC 2.3.2.27 (Polycomb Repressive Complex 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190245


  2 / 9309 MEDLINE  
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[PMID]:29337059
[Au] Autor:Lin L; Li M; Lin L; Xu X; Jiang G; Wu L
[Ad] Endereço:Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China; Tongji University School of Medicine, Shanghai 200092, China.
[Ti] Título:FPPS mediates TGF-ß1-induced non-small cell lung cancer cell invasion and the EMT process via the RhoA/Rock1 pathway.
[So] Source:Biochem Biophys Res Commun;496(2):536-541, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Farnesyl pyrophosphate synthase (FPPS), a key enzyme in the mevalonate pathway, was recently shown to play a role in cancer progression. However, its role in non-small cell lung cancer (NSCLC) metastasis and the underlying mechanism remain unclear. In this study, FPPS expression was significantly correlated with TNM stage, and metastasis. Inhibition or knockdown of FPPS blocked TGF-ß1-induced cell invasion and epithelial-to-mesenchymal transition (EMT) process. FPPS expression of FPPS was induced by TGF-ß1 and FPPS promoted cell invasion and EMT via the RhoA/Rock1 pathway. In conclusion, FPPS mediates TGF-ß1-induced lung cancer cell invasion and EMT via the RhoA/Rock1 pathway. These findings suggest new treatment strategies to reduce mortality associated with metastasis in patients with NSCLC.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Transição Epitelial-Mesenquimal
Geraniltranstransferase/metabolismo
Neoplasias Pulmonares/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
Quinases Associadas a rho/metabolismo
Proteína rhoA de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Idoso
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Linhagem Celular Tumoral
Feminino
Regulação Neoplásica da Expressão Gênica
Geraniltranstransferase/análise
Geraniltranstransferase/genética
Seres Humanos
Pulmão/metabolismo
Pulmão/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Transforming Growth Factor beta1); EC 2.5.1.10 (Geranyltranstransferase); EC 2.7.11.1 (ROCK1 protein, human); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


  3 / 9309 MEDLINE  
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[PMID]:28452702
[Au] Autor:Shin JM; Kang JH; Lee SA; Park IH; Lee HM
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Seoul, South Korea.
[Ti] Título:Effect of doxycycline on epithelial-mesenchymal transition the p38/Smad pathway in respiratory epithelial cells.
[So] Source:Am J Rhinol Allergy;31(2):71-77, 2017 Mar 01.
[Is] ISSN:1945-8932
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Doxycycline has antibacterial and anti-inflammatory effects, and it also suppresses collagen biosynthesis. This study aimed to confirm the effects and mechanism of doxycycline on transforming growth factor (TGF) beta 1 induced epithelial-mesenchymal transition and cell migration in A549 and primary nasal epithelial cells. METHODS: A 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay and phalloidin-fluorescein isothiocyanate staining were used to evaluate cytotoxicity and cellular morphologic changes. Western blot and immunofluorescence staining were used to determine the expression levels of E-cadherin, vimentin, alpha-smooth muscle actin, fibronectin, phosphorylated Smad2/3, and mitogen-activated protein kinases. Scratch and transwell migration assays were used to assess cellular migration ability. RESULTS: Doxycycline (0-10 µg/mL) had no significant cytotoxic effects in A549 and primary nasal epithelial cells. Increased expression of mesenchymal markers, including vimentin, alpha-smooth muscle actin, and fibronectin in TGF beta 1 induced A549 cells were downregulated by doxycycline treatment. In contrast, E-cadherin expression was upregulated in TGF beta 1 induced A549 cells. An in vitro cell migration assay showed that doxycycline also inhibited the ability of TGF beta 1 induced migration. Doxycycline treatment suppressed the activation of Smad2/3 and p38, whereas its inhibitory effects were similar to each element-specific inhibitor in A549 and primary nasal epithelial cells. CONCLUSION: Doxycycline inhibited TGF beta 1 induced epithelial-to-mesenchymal transition and migration by targeting Smad2/3 and p38 signal pathways in respiratory epithelial cells.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Doxiciclina/farmacologia
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Mucosa Respiratória/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células A549
Caderinas/metabolismo
Movimento Celular/efeitos dos fármacos
Regulação da Expressão Gênica
Seres Humanos
Sistema de Sinalização das MAP Quinases
Cultura Primária de Células
Mucosa Respiratória/patologia
Proteína Smad2/metabolismo
Proteína Smad3/metabolismo
Fator de Crescimento Transformador beta/metabolismo
Vimentina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cadherins); 0 (Smad2 Protein); 0 (Smad3 Protein); 0 (Transforming Growth Factor beta); 0 (Vimentin); N12000U13O (Doxycycline)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.2500/ajra.2017.31.4410


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[PMID]:29237530
[Au] Autor:Zhu XH; Li QG; Wang J; Hu GZ; Liu ZQ; Hu QH; Wu G
[Ad] Endereço:School of Medicine, Nanchang University, Nanchang 330006, China. nclqg2017@163.com.
[Ti] Título:[Mechanism of action of BET bromodomain inhibitor JQ1 in treating airway remodeling in asthmatic mice].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(12):1278-1284, 2017 Dec.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate the molecular mechanism of action of BET bromodomain inhibitor JQ1 in treating airway remodeling in asthmatic mice. METHODS: A total of 24 mice were randomly divided into control group, ovalbumin (OVA)-induced asthma group (OVA group), and JQ1 intervention group (JQ1+OVA group), with 8 mice in each group. OVA sensitization/challenge was performed to establish a mouse model of asthma. At 1 hour before challenge, the mice in the JQ1+OVA group were given intraperitoneal injection of JQ1 solution (50 µg/g). Bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected at 24 hours after the last challenge, and the total number of cells and percentage of eosinophils in BALF were calculated. Pathological staining was performed to observe histopathological changes in lung tissue. RT-PCR and Western blot were used to measure the mRNA and protein expression of E-cadherin and vimentin during epithelial-mesenchymal transition (EMT). RESULTS: Compared with the control group, the OVA group had marked infiltration of inflammatory cells in the airway, thickening of the airway wall, increased secretion of mucus, and increases in the total number of cells and percentage of eosinophils in BALF (P<0.01). Compared with the OVA group, the JQ1+OVA group had significantly alleviated airway inflammatory response and significant reductions in the total number of cells and percentage of eosinophils in BALF (P<0.01). Compared with the control group, the OVA group had significant reductions in the mRNA and protein expression of E-cadherin and significant increases in the mRNA and protein expression of vimentin (P<0.01); compared with the OVA group, the JQ1+OVA group had significant increases in the mRNA and protein expression of E-cadherin and significant reductions in the mRNA and protein expression of vimentin (P<0.01); there were no significant differences in these indices between the JQ1+OVA group and the control group (P>0.05). CONCLUSIONS: Mice with OVA-induced asthma have airway remodeling during EMT. BET bromodomain inhibitor JQ1 can reduce airway inflammation, inhibit EMT, and alleviate airway remodeling, which provides a new direction for the treatment of asthma.
[Mh] Termos MeSH primário: Remodelação das Vias Aéreas/efeitos dos fármacos
Asma/tratamento farmacológico
Azepinas/farmacologia
Triazóis/farmacologia
[Mh] Termos MeSH secundário: Animais
Caderinas/análise
Caderinas/genética
Transição Epitelial-Mesenquimal
Feminino
Camundongos
Proteínas Nucleares/antagonistas & inibidores
Ovalbumina/imunologia
RNA Mensageiro/análise
Fatores de Transcrição/antagonistas & inibidores
Vimentina/análise
Vimentina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((+)-JQ1 compound); 0 (Azepines); 0 (Brd4 protein, mouse); 0 (Cadherins); 0 (E-cadherin protein, mouse); 0 (Nuclear Proteins); 0 (RNA, Messenger); 0 (Transcription Factors); 0 (Triazoles); 0 (Vimentin); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE


  5 / 9309 MEDLINE  
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[PMID]:29190611
[Au] Autor:Liu J; Rao J; Lou X; Zhai J; Ni Z; Wang X
[Ad] Endereço:Department of Respiratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
[Ti] Título:Upregulated TRIM11 Exerts its Oncogenic Effects in Hepatocellular Carcinoma Through Inhibition of P53.
[So] Source:Cell Physiol Biochem;44(1):255-266, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The tripartite motif containing (TRIM) family plays crucial roles in tumor development and progression. However, little is known about the function and mechanism of TRIM11 in hepatocellular carcinoma (HCC). METHODS: The expression levels of TRIM11 were examined by real-time PCR, Western blot and Immunohistochemical (IHC) staining. TRIM11 knockdown cells were produced by lentivirus infection, and functional assays, such as MTT, colony formation assay, migration and invasion assays and a xenograft tumor model were used to investigate the role of TRIM11 in HCC. We also determined the effect of TRIM11 on p53 signaling and its downstream molecules. RESULTS: We found that TRIM11 mRNA and protein levels were significantly increased in HCC tissues as compared with normal tissues; increased levels correlated with poor patient survival. By loss- and gain-of-function investigations, knockdown of TRIM11 suppressed cell proliferation, migration, invasion in vitro and tumor growth in vivo. Moreover, TRIM11 negatively regulated p53 expression. Knockdown of p53 abrogated the in vitro and in vivo biological functions of TRIM11 shRNA in HCC cells. CONCLUSIONS: These data show that TRIM11 exerts its oncogenic effect in HCC by downregulating p53 both in vitro and in vivo. Our data provide new insights into the pathogenesis of HCC and indicate that TRIM11 may serve as a new therapeutic target for HCC treatment.
[Mh] Termos MeSH primário: Proteínas com Motivo Tripartido/genética
Proteínas com Motivo Tripartido/metabolismo
Proteína Supressora de Tumor p53/metabolismo
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Movimento Celular
Proliferação Celular
Ciclina D1/genética
Ciclina D1/metabolismo
Inibidor de Quinase Dependente de Ciclina p21/genética
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Inibidor de Quinase Dependente de Ciclina p27/genética
Inibidor de Quinase Dependente de Ciclina p27/metabolismo
Regulação para Baixo
Transição Epitelial-Mesenquimal
Células Hep G2
Seres Humanos
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Transplante Heterólogo
Proteínas com Motivo Tripartido/antagonistas & inibidores
Proteína Supressora de Tumor p53/antagonistas & inibidores
Proteína Supressora de Tumor p53/genética
Ubiquitina-Proteína Ligases/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (RNA, Small Interfering); 0 (TP53 protein, human); 0 (Tripartite Motif Proteins); 0 (Tumor Suppressor Protein p53); 136601-57-5 (Cyclin D1); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); EC 2.3.2.27 (TRIM11 protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1159/000484678


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[PMID]:28460469
[Au] Autor:Lam CS; Ng L; Chow AK; Wan TM; Yau S; Cheng NS; Wong SK; Man JH; Lo OS; Foo DC; Poon JT; Pang RW; Law WL
[Ad] Endereço:Division of Colorectal Surgery, Department of Surgery, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong.
[Ti] Título:Identification of microRNA 885-5p as a novel regulator of tumor metastasis by targeting CPEB2 in colorectal cancer.
[So] Source:Oncotarget;8(16):26858-26870, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer is the third most common cancer in the world and liver is the most frequent site of distant metastasis with poor prognosis. The aim of this study is to investigate microRNAs leading to liver metastasis. We applied microarray analysis and quantitative PCR to identify and validate dysregulated miRNAs in liver metastases when compared to primary CRCs. Functional significance and the underlying molecular mechanism of selected miRNA was demonstrated by a series of in vitro and in vivo assays. Our microarray analysis and subsequent quantitative PCR validation revealed that miR-885-5p was strongly up-regulated in liver metastases and in CRC cell-lines derived from distant metastases. Overexpression of miR-885-5p significantly induced cell migration, cell invasion, formation of stress fibre in vitro and development of liver and lung metastases in vivo. MiR-885-5p induced metastatic potential of CRC by repressing cytoplasmic polyadenylation element binding protein 2 transcription through directly binding to two binding sites on its 3' untranslated region, and consequently led to up-regulation of TWIST1 and hence epithelial-mesenchymal transition. Our findings demonstrated the overexpression of miR-885-5p in liver metastasis and its roles in inducing CRC metastasis, potentiating development of miR-885-5p inhibitor to treat advanced CRC in the future.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Regulação Neoplásica da Expressão Gênica
MicroRNAs/genética
Interferência de RNA
Proteínas de Ligação a RNA/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Linhagem Celular Tumoral
Movimento Celular/genética
Citoesqueleto/metabolismo
Modelos Animais de Doenças
Transição Epitelial-Mesenquimal/genética
Xenoenxertos
Seres Humanos
Neoplasias Hepáticas/secundário
Masculino
Camundongos
Metástase Neoplásica
Estadiamento de Neoplasias
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (CPEB2 protein, human); 0 (MIRN885 microRNA, human); 0 (MicroRNAs); 0 (RNA-Binding Proteins)
[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.15844


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[PMID]:27775689
[Au] Autor:Yang J; Wang T; Li Y; Yao W; Ji X; Wu Q; Han L; Han R; Yan W; Yuan J; Ni C
[Ad] Endereço:Department of Occupational Medicine and Environmental Health and Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, China.
[Ti] Título:Earthworm extract attenuates silica-induced pulmonary fibrosis through Nrf2-dependent mechanisms.
[So] Source:Lab Invest;96(12):1279-1300, 2016 12.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Silicosis is an occupational pulmonary fibrosis caused by inhalation of silica (SiO ) and there are no ideal drugs to treat this disease. Earthworm extract (EE), a natural nutrient, has been reported to have anti-inflammatory, antioxidant, and anti-apoptosis effects. The purpose of the current study was to test the protective effects of EE against SiO -induced pulmonary fibrosis and to explore the underlying mechanisms using both in vivo and in vitro models. We found that treatment with EE significantly reduced lung inflammation and fibrosis and improved lung structure and function in SiO -instilled mice. Further mechanistic investigations revealed that EE administration markedly inhibited SiO -induced oxidative stress, mitochondrial apoptotic pathway, and epithelial-mesenchymal transition in HBE and A549 cells. Furthermore, we demonstrate that Nrf2 activation partly mediates the interventional effects of EE against SiO -induced pulmonary fibrosis. Our study has identified EE to be a potential anti-oxidative, anti-inflammatory, and anti-fibrotic drug for silicosis.
[Mh] Termos MeSH primário: Antioxidantes/uso terapêutico
Modelos Animais de Doenças
Pulmão/efeitos dos fármacos
Materia Medica/uso terapêutico
Oligoquetos/química
Fibrose Pulmonar/prevenção & controle
Silicose/tratamento farmacológico
Extratos de Tecidos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/administração & dosagem
Anti-Inflamatórios não Esteroides/farmacologia
Anti-Inflamatórios não Esteroides/uso terapêutico
Antioxidantes/administração & dosagem
Antioxidantes/farmacologia
Apoptose/efeitos dos fármacos
Linhagem Celular
Células Cultivadas
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Injeções Intraperitoneais
Pulmão/metabolismo
Pulmão/patologia
Pulmão/fisiopatologia
Masculino
Materia Medica/administração & dosagem
Materia Medica/farmacologia
Camundongos Endogâmicos C57BL
Fator 2 Relacionado a NF-E2/agonistas
Fator 2 Relacionado a NF-E2/antagonistas & inibidores
Fator 2 Relacionado a NF-E2/genética
Fator 2 Relacionado a NF-E2/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Fibrose Pulmonar/etiologia
Fibrose Pulmonar/imunologia
Interferência de RNA
Distribuição Aleatória
Mucosa Respiratória/citologia
Mucosa Respiratória/efeitos dos fármacos
Mucosa Respiratória/metabolismo
Mucosa Respiratória/patologia
Silicose/metabolismo
Silicose/patologia
Silicose/fisiopatologia
Organismos Livres de Patógenos Específicos
Extratos de Tecidos/administração & dosagem
Extratos de Tecidos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antioxidants); 0 (Materia Medica); 0 (NF-E2-Related Factor 2); 0 (Tissue Extracts)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2016.101


  8 / 9309 MEDLINE  
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[PMID]:27775688
[Au] Autor:Nomura A; Majumder K; Giri B; Dauer P; Dudeja V; Roy S; Banerjee S; Saluja AK
[Ad] Endereço:Division of Surgical Oncology, Department of Surgery Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL, USA.
[Ti] Título:Inhibition of NF-kappa B pathway leads to deregulation of epithelial-mesenchymal transition and neural invasion in pancreatic cancer.
[So] Source:Lab Invest;96(12):1268-1278, 2016 12.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NF-κB has an essential role in the initiation and progression of pancreatic cancer and specifically mediates the induction of epithelial-mesenchymal transition and invasiveness. In this study, we demonstrate the importance of activated NF-κB signaling in EMT induction, lymphovascular metastasis, and neural invasion. Modulation of NF-κB activity was accomplished through the specific NF-κB inhibitor (BAY 11-7085), triptolide, and Minnelide treatment, as well as overexpression of IKBα repressor and IKK activator plasmids. In the classical lymphovascular metastatic cascade, inhibition of NF-κB decreased the expression of several EMT transcription factors (SNAI1, SNAI2, and ZEB1) and mesenchymal markers (VIM and CDH2) and decreased in vitro invasion, which was rescued by IKK activation. This was further demonstrated in vivo via BAY 11-7085 treatment in a orthotopic model of pancreatic cancer. In vivo NF-κB inhibition decreased tumor volume; decreased tumor EMT gene expression, while restoring cell-cell junctions; and decreasing overall metastasis. Furthermore, we demonstrate the importance of active NF-κB signaling in neural invasion. Triptolide treatment inhibits Nerve Growth Factor (NGF) mediated, neural-tumor co-culture in vitro invasion, and dorsal root ganglia (DRG) neural outgrowth through a disruption in tumor-neural cross talk. In vivo, Minnelide treatment decreased neurotrophin expression, nerve density, and sciatic nerve invasion. Taken together, this study demonstrates the importance of NF-κB signaling in the progression of pancreatic cancer through the modulation of EMT induction, lymphovascular invasion, and neural invasion.
[Mh] Termos MeSH primário: Transição Epitelial-Mesenquimal
NF-kappa B/metabolismo
Pâncreas/metabolismo
Neoplasias Pancreáticas/metabolismo
Nervos Periféricos/metabolismo
Neoplasias do Sistema Nervoso Periférico/secundário
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Linhagem Celular
Linhagem Celular Tumoral
Técnicas de Cocultura
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Gânglios Espinais/citologia
Gânglios Espinais/efeitos dos fármacos
Gânglios Espinais/metabolismo
Gânglios Espinais/patologia
Seres Humanos
Metástase Linfática/patologia
Metástase Linfática/prevenção & controle
Camundongos
Camundongos Nus
Inibidor de NF-kappaB alfa/genética
Inibidor de NF-kappaB alfa/metabolismo
NF-kappa B/antagonistas & inibidores
Invasividade Neoplásica/patologia
Transplante de Neoplasias
Pâncreas/efeitos dos fármacos
Pâncreas/patologia
Neoplasias Pancreáticas/tratamento farmacológico
Neoplasias Pancreáticas/patologia
Nervos Periféricos/citologia
Nervos Periféricos/efeitos dos fármacos
Nervos Periféricos/patologia
Neoplasias do Sistema Nervoso Periférico/metabolismo
Neoplasias do Sistema Nervoso Periférico/patologia
Neoplasias do Sistema Nervoso Periférico/prevenção & controle
Proteínas Recombinantes/metabolismo
Nervo Isquiático/citologia
Nervo Isquiático/efeitos dos fármacos
Nervo Isquiático/metabolismo
Nervo Isquiático/patologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (NF-kappa B); 0 (Recombinant Proteins); 139874-52-5 (NF-KappaB Inhibitor alpha)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2016.109


  9 / 9309 MEDLINE  
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Texto completo SciELO Brasil
[PMID]:29211293
[Au] Autor:Rodini CO; Lopes NM; Lara VS; Mackenzie IC
[Ad] Endereço:Universidade de São Paulo, Faculdade de Odontologia de Bauru, Departamento de Ciências Biológicas, Bauru, SP, Brasil.
[Ti] Título:Oral cancer stem cells - properties and consequences.
[So] Source:J Appl Oral Sci;25(6):708-715, 2017 Nov-Dec.
[Is] ISSN:1678-7765
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Research on cancer stem cells (CSCs) has greatly increased in the field of medicine and pathology; however, some conceptual misunderstandings are still present among the public as well as within the general scientific community that is not yet familiar with the subject. The very first problem is the misinterpretation of CSCs as a synonym of their normal counterparts, the well-known stem cells (SCs). Particularly in Dentistry, another common mistake is the misinterpretation of oral CSCs as normal tooth-derived SCs. The present review aims to clarify important concepts related to normal SCs and CSCs, as well as discuss the relevance of CSCs to the development, metastasis and therapy resistance of oral squamous cell carcinoma.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/patologia
Neoplasias Bucais/patologia
Células-Tronco Neoplásicas/patologia
[Mh] Termos MeSH secundário: Diferenciação Celular
Transformação Celular Neoplásica
Transição Epitelial-Mesenquimal
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


  10 / 9309 MEDLINE  
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[PMID]:28452807
[Au] Autor:Kim J; Kang SM; Lee HJ; Choi SY; Hong SH
[Ad] Endereço:Departments of aOral Microbiology and Immunology bOral and Maxillofacial Surgery, School of Dentistry, Kyungpook National University, Daegu, South Korea.
[Ti] Título:Oxytocin inhibits head and neck squamous cell carcinoma cell migration by early growth response-1 upregulation.
[So] Source:Anticancer Drugs;28(6):613-622, 2017 07.
[Is] ISSN:1473-5741
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The effect of oxytocin (OXT) on cancer invasion is controversial. Few studies have examined the effect of early growth response-1 (EGR1) on the invasion of head and neck squamous cell carcinoma (HNSCC). Here, we evaluated how EGR1 affects HNSCC cell migration through the molecular mechanism of OXT in exerting anti-invasion activity. Matrigel invasion and wound-healing assays were used to measure the in-vitro cell migration. The molecular mechanism of OXT was assessed by knockdown or overexpression of EGR1 in HNSCC cells. Three-dimensional (3-D) spheroids formation, followed by the image analysis for quantification was performed. OXT at 500 nmol/l increased mRNA and protein expression of E-cadherin without cytotoxicity. OXT upregulated mRNA and protein expression of EGR1 in 6 h. p53, phosphatase and tensin, and p21 expression was increased in an EGR1-dependent manner with OXT treatment. In addition, OXT significantly downregulated 3-D spheroids' formation according to spheroids' number and size. Our data showed that OXT downregulated HNSCC cell migration by EGR1 upregulation. OXT inhibited spheroids' formation of HNSCC cells under 3-D culture conditions.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/tratamento farmacológico
Movimento Celular/efeitos dos fármacos
Proteína 1 de Resposta de Crescimento Precoce/biossíntese
Neoplasias de Cabeça e Pescoço/tratamento farmacológico
Ocitocina/farmacologia
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/patologia
Transição Epitelial-Mesenquimal/efeitos dos fármacos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Neoplasias de Cabeça e Pescoço/metabolismo
Neoplasias de Cabeça e Pescoço/patologia
Seres Humanos
Invasividade Neoplásica
Metástase Neoplásica
Receptor do Fator de Crescimento Epidérmico/metabolismo
Esferoides Celulares
Células Tumorais Cultivadas
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (EGR1 protein, human); 0 (Early Growth Response Protein 1); 50-56-6 (Oxytocin); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1097/CAD.0000000000000501



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