Base de dados : MEDLINE
Pesquisa : E05.624 [Categoria DeCS]
Referências encontradas : 45954 [refinar]
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[PMID]:28922779
[Au] Autor:Hanley CJ; Mellone M; Ford K; Thirdborough SM; Mellows T; Frampton SJ; Smith DM; Harden E; Szyndralewiez C; Bullock M; Noble F; Moutasim KA; King EV; Vijayanand P; Mirnezami AH; Underwood TJ; Ottensmeier CH; Thomas GJ
[Ad] Endereço:Cancer Sciences Unit, University of Southampton Faculty of Medicine, Southampton, UK; Genkyotex SA, Plan-les-Ouates, Switzerland; La Jolla Institute for Allergy and Immunology, La Jolla, CA.
[Ti] Título:Targeting the Myofibroblastic Cancer-Associated Fibroblast Phenotype Through Inhibition of NOX4.
[So] Source:J Natl Cancer Inst;110(1), 2018 Jan 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Cancer-associated fibroblasts (CAFs) are tumor-promoting and correlate with poor survival in many cancers, which has led to their emergence as potential therapeutic targets. However, effective methods to manipulate these cells clinically have yet to be developed. Methods: CAF accumulation and prognostic significance in head and neck cancer (oral, n = 260; oropharyngeal, n = 271), and colorectal cancer (n = 56) was analyzed using immunohistochemistry. Mechanisms regulating fibroblast-to-myofibroblast transdifferentiation were investigated in vitro using RNA interference/pharmacological inhibitors followed by polymerase chain reaction (PCR), immunoblotting, immunofluorescence, and functional assays. RNA sequencing/bioinformatics and immunohistochemistry were used to analyze NAD(P)H Oxidase-4 (NOX4) expression in different human tumors. NOX4's role in CAF-mediated tumor progression was assessed in vitro, using CAFs from multiple tissues in Transwell and organotypic culture assays, and in vivo, using xenograft (n = 9-15 per group) and isograft (n = 6 per group) tumor models. All statistical tests were two-sided. Results: Patients with moderate/high levels of myofibroblastic-CAF had a statistically significant decrease in cancer-specific survival rates in each cancer type analyzed (hazard ratios [HRs] = 1.69-7.25, 95% confidence intervals [CIs] = 1.11 to 31.30, log-rank P ≤ .01). Fibroblast-to-myofibroblast transdifferentiation was dependent on a delayed phase of intracellular reactive oxygen species, generated by NOX4, across different anatomical sites and differentiation stimuli. A statistically significant upregulation of NOX4 expression was found in multiple human cancers (P < .001), strongly correlating with myofibroblastic-CAFs (r = 0.65-0.91, adjusted P < .001). Genetic/pharmacological inhibition of NOX4 was found to revert the myofibroblastic-CAF phenotype ex vivo (54.3% decrease in α-smooth muscle actin [α-SMA], 95% CI = 10.6% to 80.9%, P = .009), prevent myofibroblastic-CAF accumulation in vivo (53.2%-79.0% decrease in α-SMA across different models, P ≤ .02) and slow tumor growth (30.6%-64.0% decrease across different models, P ≤ .04). Conclusions: These data suggest that pharmacological inhibition of NOX4 may have broad applicability for stromal targeting across cancer types.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Fibroblastos Associados a Câncer/patologia
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Carcinoma de Células Escamosas/tratamento farmacológico
Neoplasias Colorretais/química
Neoplasias Esofágicas/tratamento farmacológico
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Bucais/química
Miofibroblastos/patologia
NADPH Oxidases/antagonistas & inibidores
Neoplasias Orofaríngeas/química
[Mh] Termos MeSH secundário: Actinas/análise
Adenocarcinoma/química
Adenocarcinoma/genética
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Fibroblastos Associados a Câncer/química
Fibroblastos Associados a Câncer/fisiologia
Carcinoma Pulmonar de Células não Pequenas/química
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma de Células Escamosas/química
Carcinoma de Células Escamosas/genética
Contagem de Células
Transdiferenciação Celular/efeitos dos fármacos
Transdiferenciação Celular/genética
Neoplasias Colorretais/patologia
Progressão da Doença
Neoplasias Esofágicas/química
Neoplasias Esofágicas/genética
Feminino
Neoplasias de Cabeça e Pescoço/química
Neoplasias de Cabeça e Pescoço/tratamento farmacológico
Neoplasias de Cabeça e Pescoço/genética
Seres Humanos
Neoplasias Pulmonares/química
Neoplasias Pulmonares/genética
Masculino
Camundongos
Meia-Idade
Neoplasias Bucais/patologia
Miofibroblastos/química
NADPH Oxidase 4
NADPH Oxidases/análise
NADPH Oxidases/genética
Transplante de Neoplasias
Neoplasias Orofaríngeas/patologia
Fenótipo
Pirazóis/uso terapêutico
Piridinas/uso terapêutico
Interferência de RNA
Espécies Reativas de Oxigênio/metabolismo
Taxa de Sobrevida
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (GKT137831); 0 (Pyrazoles); 0 (Pyridines); 0 (Reactive Oxygen Species); EC 1.6.3.- (NADPH Oxidase 4); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.- (NOX4 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx121


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[PMID]:28903484
[Au] Autor:Yang Y; Gao X; Zhang M; Yan S; Sun C; Xiao F; Huang N; Yang X; Zhao K; Zhou H; Huang S; Xie B; Zhang N
[Ad] Endereço:Department of Neurosurgery, The 1st Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong Province, PR China; Guangdong Provincial Key Laboratory of Pituitary Tumor, Guangzhou, Guangdong Province, PR China; Department of Scientific Research Section, The 1st Affiliated Hospital of Sun Y
[Ti] Título:Novel Role of FBXW7 Circular RNA in Repressing Glioma Tumorigenesis.
[So] Source:J Natl Cancer Inst;110(3), 2018 Mar 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Circular RNAs (circRNAs) are RNA transcripts that are widespread in the eukaryotic genome. Recent evidence indicates that circRNAs play important roles in tissue development, gene regulation, and carcinogenesis. However, whether circRNAs encode functional proteins remains elusive, although translation of several circRNAs was recently reported. Methods: CircRNA deep sequencing was performed by using 10 pathologically diagnosed glioblastoma samples and their paired adjacent normal brain tissues. Northern blotting, Sanger sequencing, antibody, and liquid chromatograph Tandem Mass Spectrometer were used to confirm the existence of circ-FBXW7 and its encoded protein in in two cell lines. Lentivirus-transfected stable U251 and U373 cells were used to assess the biological functions of the novel protein invitro and invivo (five mice per group). Clinical implications of circ-FBXW7 were assessed in 38 pathologically diagnosed glioblastoma samples and their paired periphery normal brain tissues by using quantitative polymerase chain reaction (two-sided log-rank test). Results: Circ-FBXW7 is abundantly expressed in the normal human brain (reads per kilobase per million mapped reads [RPKM] = 9.31). The spanning junction open reading frame in circ-FBXW7 driven by internal ribosome entry site encodes a novel 21-kDa protein, which we termed FBXW7-185aa. Upregulation of FBXW7-185aa in cancer cells inhibited proliferation and cell cycle acceleration, while knockdown of FBXW7-185aa promoted malignant phenotypes invitro and invivo. FBXW7-185aa reduced the half-life of c-Myc by antagonizing USP28-induced c-Myc stabilization. Moreover, circ-FBXW7 and FBXW7-185aa levels were reduced in glioblastoma clinical samples compared with their paired tumor-adjacent tissues (P < .001). Circ-FBXW7 expression positively associated with glioblastoma patient overall survival (P = .03). Conclusions: Endogenous circRNA encodes a functional protein in human cells, and circ-FBXW7 and FBXW7-185aa have potential prognostic implications in brain cancer.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/genética
Proteínas de Ciclo Celular/genética
Transformação Celular Neoplásica/genética
Proteínas F-Box/genética
Glioblastoma/genética
RNA/análise
Ubiquitina-Proteína Ligases/genética
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Neoplasias Encefálicas/química
Ciclo Celular/genética
Proteínas de Ciclo Celular/análise
Linhagem Celular Tumoral
Proliferação Celular/genética
Proteínas F-Box/análise
Proteína 7 com Repetições F-Box-WD
Feminino
Glioblastoma/química
Meia-Vida
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Transplante de Neoplasias
Fases de Leitura Aberta
Proteínas Proto-Oncogênicas c-myc/metabolismo
Análise de Sequência de RNA
Taxa de Sobrevida
Ubiquitina Tiolesterase/metabolismo
Ubiquitina-Proteína Ligases/análise
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (F-Box Proteins); 0 (F-Box-WD Repeat-Containing Protein 7); 0 (FBXW7 protein, human); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, circular); 63231-63-0 (RNA); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.1.2.15 (USP28 protein, human); EC 3.4.19.12 (Ubiquitin Thiolesterase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx166


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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


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[PMID]:29442000
[Au] Autor:Li YL; Zhao YG; Chen B; Li XF
[Ti] Título:MicroRNA-132 sensitizes nasopharyngeal carcinoma cells to cisplatin through regulation of forkhead box A1 protein.
[So] Source:Pharmazie;71(12):715-718, 2016 Dec 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Chemoresistance in cancer is one of the major hindrances in cisplatin (DPP) treatment for nasopharyngeal carcinoma (NPC). The mechanism of such resistance remains unknown. Therefore, the present study aimed to clarify the mechanism of DDP resistance and attempted to reduce chemoresistance. Here, we found that miR-132, as a tumor suppressor, was poorly expressed in a cisplatin resistant CNE2 cell line (CNE2/DPP) accompanied with a decreased expression of miR-132 and an increased expression of FOXA1 compared with the parental cells CNE2. Exogenous overexpression of miR-132 in CNE2/DPP could sensitize their reaction to the treatment of cisplatin. In addition, FOXA1 knockdown in CNE2/DPP cells increased the chemosensitivity to DPP, suggesting the dependence of FOXA1 regulation in miR-132 activity. Moreover, miR-132 can restore cisplatin treatment response in cisplatin-resistant xenografts in vivo, while FOXA1 protein levels were decreased. In summary, our results provide novel mechanistic insights into the role of miR-132/FOXA1 signaling in the cisplatin resistance of NPC cells. Targeting of miR-132 is a potential therapeutic approach for NPC.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Carcinoma/tratamento farmacológico
Cisplatino/farmacologia
Fator 3-alfa Nuclear de Hepatócito/efeitos dos fármacos
Fator 3-alfa Nuclear de Hepatócito/metabolismo
MicroRNAs/farmacologia
Neoplasias Nasofaríngeas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos
Feminino
Técnicas de Silenciamento de Genes
Seres Humanos
Camundongos
Camundongos Nus
Transplante de Neoplasias
Interferência de RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Hepatocyte Nuclear Factor 3-alpha); 0 (MIRN132 microRNA, mouse); 0 (MicroRNAs); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6764


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[PMID]:28456746
[Au] Autor:Carretta M; de Boer B; Jaques J; Antonelli A; Horton SJ; Yuan H; de Bruijn JD; Groen RWJ; Vellenga E; Schuringa JJ
[Ad] Endereço:Department of Experimental Hematology, Cancer Research Centre Groningen, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands.
[Ti] Título:Genetically engineered mesenchymal stromal cells produce IL-3 and TPO to further improve human scaffold-based xenograft models.
[So] Source:Exp Hematol;51:36-46, 2017 07.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Recently, NOD-SCID IL2Rγ (NSG) mice were implanted with human mesenchymal stromal cells (MSCs) in the presence of ceramic scaffolds or Matrigel to mimic the human bone marrow (BM) microenvironment. This approach allowed the engraftment of leukemic samples that failed to engraft in NSG mice without humanized niches and resulted in a better preservation of leukemic stem cell self-renewal properties. To further improve our humanized niche scaffold model, we genetically engineered human MSCs to secrete human interleukin-3 (IL-3) and thrombopoietin (TPO). In vitro, these IL-3- and TPO-producing MSCs were superior in expanding human cord blood (CB) CD34 hematopoietic stem/progenitor cells. MLL-AF9-transduced CB CD34 cells could be transformed efficiently along myeloid or lymphoid lineages on IL-3- and TPO-producing MSCs. In vivo, these genetically engineered MSCs maintained their ability to differentiate into bone, adipocytes, and other stromal components. Upon transplantation of MLL-AF9-transduced CB CD34 cells, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) developed in engineered scaffolds, in which a significantly higher percentage of myeloid clones was observed in the mouse compartments compared with previous models. Engraftment of primary AML, B-cell ALL, and biphenotypic acute leukemia (BAL) patient samples was also evaluated, and all patient samples could engraft efficiently; the myeloid compartment of the BAL samples was better preserved in the human cytokine scaffold model. In conclusion, we show that we can genetically engineer the ectopic human BM microenvironment in a humanized scaffold xenograft model. This approach will be useful for functional study of the importance of niche factors in normal and malignant human hematopoiesis.
[Mh] Termos MeSH primário: Diferenciação Celular
Engenharia Genética
Interleucina-3
Células Mesenquimais Estromais/metabolismo
Nicho de Células-Tronco
Trombopoetina
Tecidos Suporte/química
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Xenoenxertos
Seres Humanos
Interleucina-3/biossíntese
Interleucina-3/genética
Leucemia Mieloide Aguda/genética
Leucemia Mieloide Aguda/metabolismo
Transplante de Células-Tronco Mesenquimais
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Transplante de Neoplasias
Leucemia-Linfoma Linfoblástico de Células Precursoras B/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras B/metabolismo
Trombopoetina/biossíntese
Trombopoetina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL3 protein, human); 0 (Interleukin-3); 9014-42-0 (Thrombopoietin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180224
[Lr] Data última revisão:
180224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:29335551
[Au] Autor:Fang T; Lv H; Lv G; Li T; Wang C; Han Q; Yu L; Su B; Guo L; Huang S; Cao D; Tang L; Tang S; Wu M; Yang W; Wang H
[Ad] Endereço:International Co-operation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute, Second Military Medical University, Shanghai, 200438, China.
[Ti] Título:Tumor-derived exosomal miR-1247-3p induces cancer-associated fibroblast activation to foster lung metastasis of liver cancer.
[So] Source:Nat Commun;9(1):191, 2018 01 15.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The communication between tumor-derived elements and stroma in the metastatic niche has a critical role in facilitating cancer metastasis. Yet, the mechanisms tumor cells use to control metastatic niche formation are not fully understood. Here we report that in the lung metastatic niche, high-metastatic hepatocellular carcinoma (HCC) cells exhibit a greater capacity to convert normal fibroblasts to cancer-associated fibroblasts (CAFs) than low-metastatic HCC cells. We show high-metastatic HCC cells secrete exosomal miR-1247-3p that directly targets B4GALT3, leading to activation of ß1-integrin-NF-κB signaling in fibroblasts. Activated CAFs further promote cancer progression by secreting pro-inflammatory cytokines, including IL-6 and IL-8. Clinical data show high serum exosomal miR-1247-3p levels correlate with lung metastasis in HCC patients. These results demonstrate intercellular crosstalk between tumor cells and fibroblasts is mediated by tumor-derived exosomes that control lung metastasis of HCC, providing potential targets for prevention and treatment of cancer metastasis.
[Mh] Termos MeSH primário: Fibroblastos Associados a Câncer/metabolismo
Carcinoma Hepatocelular/metabolismo
Exossomos/metabolismo
Regulação Neoplásica da Expressão Gênica
Neoplasias Hepáticas/metabolismo
Neoplasias Pulmonares/metabolismo
MicroRNAs/genética
N-Acetil-Lactosamina Sintase/genética
[Mh] Termos MeSH secundário: Animais
Fibroblastos Associados a Câncer/patologia
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/secundário
Comunicação Celular
Linhagem Celular Tumoral
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/patologia
Exossomos/química
Seres Humanos
Integrina beta1/genética
Integrina beta1/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Interleucina-8/genética
Interleucina-8/metabolismo
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/secundário
Masculino
Camundongos
Camundongos Nus
MicroRNAs/secreção
N-Acetil-Lactosamina Sintase/metabolismo
Invasividade Neoplásica
Transplante de Neoplasias
Células Neoplásicas Circulantes/metabolismo
Células Neoplásicas Circulantes/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL6 protein, human); 0 (Integrin beta1); 0 (Interleukin-6); 0 (Interleukin-8); 0 (MIRN1247 microRNA, human); 0 (MicroRNAs); EC 2.4.1.90 (N-Acetyllactosamine Synthase)
[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:180117
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02583-0


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[PMID]:27779108
[Au] Autor:D'Alesio C; Punzi S; Cicalese A; Fornasari L; Furia L; Riva L; Carugo A; Curigliano G; Criscitiello C; Pruneri G; Pelicci PG; Faretta M; Bossi D; Lanfrancone L
[Ad] Endereço:Department of Experimental Oncology, European Institute of Oncology, Milan 20141, Italy.
[Ti] Título:RNAi screens identify CHD4 as an essential gene in breast cancer growth.
[So] Source:Oncotarget;7(49):80901-80915, 2016 Dec 06.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epigenetic regulation plays an essential role in tumor development and epigenetic modifiers are considered optimal potential druggable candidates. In order to identify new breast cancer vulnerabilities and improve therapeutic chances for patients, we performed in vivo and in vitro shRNA screens in a human breast cancer cell model (MCF10DCIS.com cell line) using epigenetic libraries. Among the genes identified in our screening, we deeply investigated the role of Chromodomain Helicase DNA binding Protein 4 (CHD4) in breast cancer tumorigenesis. CHD4 silencing significantly reduced tumor growth in vivo and proliferation in vitro of MCF10DCIS.com cells. Similarly, in vivo breast cancer growth was decreased in a spontaneous mouse model of breast carcinoma (MMTV-NeuT system) and in metastatic patient-derived xenograft models. Conversely, no reduction in proliferative ability of non-transformed mammary epithelial cells (MCF10A) was detected. Moreover, we showed that CHD4 depletion arrests proliferation by inducing a G0/G1 block of cell cycle associated with up-regulation of CDKN1A (p21). These results highlight the relevance of genetic screens in the identification of tumor frailties and the role of CHD4 as a potential pharmacological target to inhibit breast cancer growth.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Proliferação Celular
DNA Helicases/genética
Complexo Mi-2 de Remodelação de Nucleossomo e Desacetilase/genética
Interferência de RNA
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/enzimologia
Neoplasias da Mama/patologia
Pontos de Checagem do Ciclo Celular
Linhagem Celular Tumoral
Biologia Computacional
Inibidor de Quinase Dependente de Ciclina p21/genética
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
DNA Helicases/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica
Biblioteca Gênica
Redes Reguladoras de Genes
Predisposição Genética para Doença
Seres Humanos
Complexo Mi-2 de Remodelação de Nucleossomo e Desacetilase/metabolismo
Camundongos Endogâmicos NOD
Camundongos SCID
Transplante de Neoplasias
Fenótipo
Transdução de Sinais
Fatores de Tempo
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN1A protein, human); 0 (CHD4 protein, human); 0 (Cdkn1a protein, mouse); 0 (Cyclin-Dependent Kinase Inhibitor p21); EC 3.5.1.98 (Mi-2 Nucleosome Remodeling and Deacetylase Complex); EC 3.6.1.3 (Mi-2beta protein, mouse); EC 3.6.4.- (DNA Helicases)
[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:161026
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.12646


  8 / 45954 MEDLINE  
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[PMID]:29217194
[Au] Autor:Kong Q; Qiu M
[Ad] Endereço:Department of Oncology, Affiliated Hospital of Jining Medical College, Jining, 272029, Shangdong province, China.
[Ti] Título:Long noncoding RNA SNHG15 promotes human breast cancer proliferation, migration and invasion by sponging miR-211-3p.
[So] Source:Biochem Biophys Res Commun;495(2):1594-1600, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Long non-coding RNAs (lncRNA) have been demonstrated to act as essential regulators in the development and progression of breast cancer. In our study, we found that long noncoding RNA SNHG15 was highly expressed in breast cancer tissues and cell lines. And the expression of SNHG15 was correlated with TNM stage, lymphnode metastasis and survival in breast cancer patients. SNHG15 knockdown significantly inhibited the proliferation and induced apoptosis in breast cancer cells in vitro and in vivo. Besides, SNHG15 downregulation suppressed cell migration and invasion in MCF-7 and BT-20 cells, and inhibited epithelial-mesenchymal transition (EMT). In mechanism, we found that SNHG15 acted as a competing endogenous RNA to sponge miR-211-3p, which was downregulated in breast cancers and inhibited cell proliferation and migration. Our results showed that there was a negative correlation between SNHG15 and miR-211-3p expression in breast cancer patients. Collectively, we, for the first time, revealed the functions of SNHG15 and miR-211-3p in breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Neoplasias da Mama/patologia
MicroRNAs/genética
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Neoplasias da Mama/metabolismo
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Progressão da Doença
Transição Epitelial-Mesenquimal/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Técnicas de Silenciamento de Genes
Xenoenxertos
Seres Humanos
Células MCF-7
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
MicroRNAs/metabolismo
Invasividade Neoplásica/genética
Transplante de Neoplasias
RNA Longo não Codificante/antagonistas & inibidores
RNA Longo não Codificante/metabolismo
RNA Neoplásico/antagonistas & inibidores
RNA Neoplásico/genética
RNA Neoplásico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN211 microRNA, human); 0 (MicroRNAs); 0 (RNA, Long Noncoding); 0 (RNA, Neoplasm); 0 (SNHG16 lncRNA, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE


  9 / 45954 MEDLINE  
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[PMID]:27775704
[Au] Autor:Brasó-Maristany F; Filosto S; Catchpole S; Marlow R; Quist J; Francesch-Domenech E; Plumb DA; Zakka L; Gazinska P; Liccardi G; Meier P; Gris-Oliver A; Cheang MC; Perdrix-Rosell A; Shafat M; Noël E; Patel N; McEachern K; Scaltriti M; Castel P; Noor F; Buus R; Mathew S; Watkins J; Serra V; Marra P; Grigoriadis A; Tutt AN
[Ad] Endereço:Breast Cancer Now Research Unit, Division of Cancer Studies, Faculty of Life Sciences and Medicine, King's College London, Guy's Hospital, London, UK.
[Ti] Título:PIM1 kinase regulates cell death, tumor growth and chemotherapy response in triple-negative breast cancer.
[So] Source:Nat Med;22(11):1303-1313, 2016 11.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Triple-negative breast cancers (TNBCs) have poor prognosis and lack targeted therapies. Here we identified increased copy number and expression of the PIM1 proto-oncogene in genomic data sets of patients with TNBC. TNBC cells, but not nonmalignant mammary epithelial cells, were dependent on PIM1 for proliferation and protection from apoptosis. PIM1 knockdown reduced expression of the anti-apoptotic factor BCL2, and dynamic BH3 profiling of apoptotic priming revealed that PIM1 prevents mitochondrial-mediated apoptosis in TNBC cell lines. In TNBC tumors and their cellular models, PIM1 expression was associated with several transcriptional signatures involving the transcription factor MYC, and PIM1 depletion in TNBC cell lines decreased, in a MYC-dependent manner, cell population growth and expression of the MYC target gene MCL1. Treatment with the pan-PIM kinase inhibitor AZD1208 impaired the growth of both cell line and patient-derived xenografts and sensitized them to standard-of-care chemotherapy. This work identifies PIM1 as a malignant-cell-selective target in TNBC and the potential use of PIM1 inhibitors for sensitizing TNBC to chemotherapy-induced apoptotic cell death.
[Mh] Termos MeSH primário: Apoptose/genética
Proliferação Celular/genética
Regulação Neoplásica da Expressão Gênica
Proteínas Proto-Oncogênicas c-pim-1/genética
Neoplasias de Mama Triplo Negativas/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Compostos de Bifenilo/farmacologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Variações do Número de Cópias de DNA
Feminino
Técnicas de Silenciamento de Genes
Seres Humanos
Camundongos
Mitocôndrias/metabolismo
Proteína de Sequência 1 de Leucemia de Células Mieloides/metabolismo
Transplante de Neoplasias
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Proteínas Proto-Oncogênicas c-myc/metabolismo
Proteínas Proto-Oncogênicas c-pim-1/antagonistas & inibidores
Reação em Cadeia da Polimerase em Tempo Real
Tiazolidinas/farmacologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (AZD1208); 0 (BCL2 protein, human); 0 (Biphenyl Compounds); 0 (MCL1 protein, human); 0 (MYC protein, human); 0 (Myeloid Cell Leukemia Sequence 1 Protein); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Proto-Oncogene Proteins c-myc); 0 (Thiazolidines); EC 2.7.11.1 (PIM1 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-pim-1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4198


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[PMID]:29193658
[Au] Autor:Imawari Y; Mimoto R; Hirooka S; Morikawa T; Takeyama H; Yoshida K
[Ad] Endereço:Department of Biochemistry, Jikei University School of Medicine, Tokyo, Japan.
[Ti] Título:Downregulation of dual-specificity tyrosine-regulated kinase 2 promotes tumor cell proliferation and invasion by enhancing cyclin-dependent kinase 14 expression in breast cancer.
[So] Source:Cancer Sci;109(2):363-372, 2018 Feb.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumor progression is the main cause of death in patients with breast cancer. Accumulating evidence suggests that dual-specificity tyrosine-regulated kinase 2 (DYRK2) functions as a tumor suppressor by regulating cell survival, differentiation, proliferation and apoptosis. However, little is known about the mechanisms of transcriptional regulation by DYRK2 in cancer progression, particularly with respect to cancer proliferation and invasion. Here, using a comprehensive expression profiling approach, we show that cyclin-dependent kinase 14 (CDK14) is a target of DYRK2. We found that reduced DYRK2 expression increases CDK14 expression, which promotes cancer cell proliferation and invasion in vitro, in addition to tumorigenicity in vivo. CDK14 and DYRK2 expression inversely correlated in human breast cancer tissues. We further identified androgen receptor (AR) as a candidate of DYRK2-dependent transcription factors regulating CDK14. Taken together, our findings suggest a mechanism by which DYRK2 controls CDK14 expression to regulate tumor cell proliferation and invasion in breast cancer. Targeting of this pathway may be a promising therapeutic strategy for treating breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Quinases Ciclina-Dependentes/genética
Proteínas Serina-Treonina Quinases/genética
Proteínas Tirosina Quinases/genética
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/genética
Neoplasias da Mama/metabolismo
Proliferação Celular
Quinases Ciclina-Dependentes/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica
Técnicas de Silenciamento de Genes
Seres Humanos
Células MCF-7
Camundongos
Invasividade Neoplásica
Transplante de Neoplasias
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Tirosina Quinases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.1.- (Dyrk kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.22 (CDK14 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13459



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