Base de dados : MEDLINE
Pesquisa : D12.644.360.262.150.100 [Categoria DeCS]
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[PMID]:29441916
[Au] Autor:Fan X; Wang P; Sun Y; Jiang J; Du H; Wang Z; Duan Z; Lei H; Li H
[Ti] Título:Oleanolic acid derivatives inhibit the Wnt/ß-catenin signaling pathway by promoting the phosphorylation of ß-catenin in human SMMC-7721 cells.
[So] Source:Pharmazie;71(7):398-401, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Oleanolic acid, isolated from privet, has shown antitumor effects in several cancers. However, the underlying molecular mechanism associated with these effects is largely unknown. In this study, we explored the effect of oleanolic acid derivatives on the Wnt/ß-catenin signaling pathway in human hepatocellular carcinoma SMMC-7721 cells. The mRNA and protein levels of related genes were determined by real-time quantitative PCR and Western blot, respectively. Treatment of SMMC-7721 cells with oleanolic acid derivatives led to the downregulation of the mRNA and protein levels of ß-catenin, c-myc, and cyclin D1. Treatment with oleanolic acid derivatives decreased the levels of ß-catenin in both the cytoplasm and the nucleus. Moreover, oleanolic acid derivatives promoted the phosphorylation of ß-catenin (Ser33/37/Thr41) in the cytoplasm. Our results suggest that oleanolic acid derivatives inhibit the Wnt/ß-catenin signaling pathway by stimulating the phosphorylation of ß-catenin (Ser33/37/Thr41) in human SMMC-7721 cells.
[Mh] Termos MeSH primário: Ácido Oleanólico/análogos & derivados
Ácido Oleanólico/farmacologia
Via de Sinalização Wnt/efeitos dos fármacos
beta Catenina/efeitos dos fármacos
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Núcleo Celular/efeitos dos fármacos
Núcleo Celular/metabolismo
Ciclina D1/antagonistas & inibidores
Ciclina D1/biossíntese
Citoplasma/efeitos dos fármacos
Citoplasma/metabolismo
Regulação para Baixo/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-myc/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-myc/biossíntese
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CTNNB1 protein, human); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, Messenger); 0 (beta Catenin); 136601-57-5 (Cyclin D1); 6SMK8R7TGJ (Oleanolic Acid)
[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:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6536


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[PMID]:28453729
[Au] Autor:Chen Z; Xie J; Hao H; Lin H; Wang L; Zhang Y; Chen L; Cao S; Huang X; Liao W; Bin J; Liao Y
[Ad] Endereço:State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, 1838, Guangzhou Avenue North, Guangzhou 510515, China.
[Ti] Título:Ablation of periostin inhibits post-infarction myocardial regeneration in neonatal mice mediated by the phosphatidylinositol 3 kinase/glycogen synthase kinase 3ß/cyclin D1 signalling pathway.
[So] Source:Cardiovasc Res;113(6):620-632, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: To resolve the controversy as to whether periostin plays a role in myocardial regeneration after myocardial infarction (MI), we created a neonatal mouse model of MI to investigate the influence of periostin ablation on myocardial regeneration and clarify the underlying mechanisms. Methods and results: Neonatal periostin-knockout mice and their wildtype littermates were subjected to MI or sham surgery. In the wildtype mice after MI, fibrosis was detectable at 3 days and fibrotic tissue was completely replaced by regenerated myocardium at 21 days. In contrast, in the knockout mice, significant fibrosis in the infarcted area was present at even 3 weeks after MI. Levels of phosphorylated-histone 3 and aurora B in the myocardium, detected by immunofluorescence and western blotting, were significantly lower in knockout than in wildtype mice at 7 days after MI. Similarly, angiogenesis was decreased in the knockout mice after MI. Expression of both the endothelial marker CD-31 and α-smooth muscle actin was markedly lower in the knockout than in wildtype mice at 7 days after MI. The knockout MI group had elevated levels of glycogen synthase kinase (GSK) 3ß and decreased phosphatidylinositol 3-kinase (PI3K), phosphorylated serine/threonine protein kinase B (p-Akt), and cyclin D1, compared with the wildtype MI group. Similar effects were observed in experiments using cultured cardiomyocytes from neonatal wildtype or periostin knockout mice. Administration of SB216763, a GSK3ß inhibitor, to knockout neonatal mice decreased myocardial fibrosis and increased angiogenesis in the infarcted area after MI. Conclusion: Ablation of periostin suppresses post-infarction myocardial regeneration by inhibiting the PI3K/GSK3ß/cyclin D1 signalling pathway, indicating that periostin is essential for myocardial regeneration.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/deficiência
Ciclina D1/metabolismo
Infarto do Miocárdio/enzimologia
Miocárdio/enzimologia
Fosfatidilinositol 3-Quinase/metabolismo
Regeneração
Proteínas Repressoras/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Moléculas de Adesão Celular/genética
Células Cultivadas
Modelos Animais de Doenças
Fibrose
Camundongos Knockout
Infarto do Miocárdio/genética
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Miocárdio/patologia
Neovascularização Fisiológica
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Regeneração/efeitos dos fármacos
Proteínas Repressoras/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccnd1 protein, mouse); 0 (Cell Adhesion Molecules); 0 (GSKIP protein, mouse); 0 (Postn protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Repressor Proteins); 136601-57-5 (Cyclin D1); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx001


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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]:29378551
[Au] Autor:Fu X; Li S; Zhou S; Wu Q; Jin F; Shi J
[Ad] Endereço:Joint International Research Laboratory of Ethnomedicine, Zunyi Medical College, Zunyi, Guizhou, China.
[Ti] Título:Stimulatory effect of icariin on the proliferation of neural stem cells from rat hippocampus.
[So] Source:BMC Complement Altern Med;18(1):34, 2018 Jan 29.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Icariin (ICA), a major ingredient of Epimediumbrevicornum, has various pharmacological activities including central nervous system protective functions such as the improvement of learning and memory function in mice models of Alzheimer's disease. It has been reported that ICA can promote regeneration of peripheral nerve and functional recovery. The purpose of this study was to investigate the potentiating effect of ICA on the proliferation of rat hippocampal neural stem cells, and explore the possible mechanism involved. METHODS: Primary neural stem cells were prepared from the hippocampus of newly born SD rats, and cells were cultured in special stem cell culture medium. Neural stem cells were confirmed by immunofluorescence detection of nestin, NSE and GFAP expression. The effect of ICA on the growth and proliferation of the neural stem cells was evaluated by 5-ethynyl-2-deoxyuridine (EdU) labeling of proliferating cells, and photomicrographic images of the cultured neural stem cells. Further, the mechanism of ICA-induced cell proliferation of neural stem cells was investigated by analyzing the gene and protein expression of cell cycle related genes cyclin D1 and p21. RESULTS: The present study showed that icariin promotes the growth and proliferation of neural stem cells from rat hippocampus in a dose-dependent manner. Incubation of cells with icariin resulted in significant increase in the number of stem cell spheres as well as the increased incorporation of EdU when compared with cells exposed to control vehicle. In addition, it was found that icariin-induced effect on neural stem cells is associated with increased mRNA and protein expression of cell cycle genes cyclin D1 and p21. CONCLUSIONS: This study evidently demonstrates the potentiating effect of ICA on neural stem cell growth and proliferation, which might be mediated through regulation of cell cycle gene and protein expression promoting cell cycle progression.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Flavonoides/farmacologia
Hipocampo/citologia
Células-Tronco Neurais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Ciclina D1/metabolismo
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Células-Tronco Neurais/citologia
Células-Tronco Neurais/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (Flavonoids); 136601-57-5 (Cyclin D1); VNM47R2QSQ (icariin)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-018-2095-y


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[PMID]:28460446
[Au] Autor:Kapil S; Sharma BK; Patil M; Elattar S; Yuan J; Hou SX; Kolhe R; Satyanarayana A
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Molecular Oncology & Biomarkers Program, Georgia Cancer Center, Augusta University, Augusta, GA 30912, USA.
[Ti] Título:The cell polarity protein Scrib functions as a tumor suppressor in liver cancer.
[So] Source:Oncotarget;8(16):26515-26531, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Scrib is a membrane protein that is involved in the maintenance of apical-basal cell polarity of the epithelial tissues. However, Scrib has also been shown to be mislocalized to the cytoplasm in breast and prostate cancer. Here, for the first time, we report that Scrib not only translocates to the cytoplasm but also to the nucleus in hepatocellular carcinoma (HCC) cells, and in mouse and human liver tumor samples. We demonstrate that Scrib overexpression suppresses the growth of HCC cells in vitro, and Scrib deficiency enhances liver tumor growth in vivo. At the molecular level, we have identified the existence of a positive feed-back loop between Yap1 and c-Myc in HCC cells, which Scrib disrupts by simultaneously regulating the MAPK/ERK and Hippo signaling pathways. Overall, Scrib inhibits liver cancer cell proliferation by suppressing the expression of three oncogenes, Yap1, c-Myc and cyclin D1, thereby functioning as a tumor suppressor in liver cancer.
[Mh] Termos MeSH primário: Neoplasias Hepáticas/metabolismo
Proteínas de Membrana/metabolismo
Proteínas Supressoras de Tumor/metabolismo
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Proteínas Adaptadoras de Transdução de Sinal/genética
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Ciclo Celular/genética
Linhagem Celular Tumoral
Proliferação Celular
Transformação Celular Neoplásica/induzido quimicamente
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Ciclina D1/genética
Ciclina D1/metabolismo
Modelos Animais de Doenças
Expressão Gênica
Xenoenxertos
Seres Humanos
Neoplasias Hepáticas/genética
Sistema de Sinalização das MAP Quinases
Proteínas de Membrana/genética
Camundongos
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Ligação Proteica
Transporte Proteico
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Proto-Oncogênicas c-myc/genética
Proteínas Proto-Oncogênicas c-myc/metabolismo
Transdução de Sinais
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Membrane Proteins); 0 (Phosphoproteins); 0 (Proto-Oncogene Proteins c-myc); 0 (SCRIB protein, human); 0 (Tumor Suppressor Proteins); 0 (YAP1 (Yes-associated) protein, human); 136601-57-5 (Cyclin D1); EC 2.7.11.1 (Hippo protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[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.15713


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[PMID]:29332262
[Au] Autor:Karpinsky G; Krawczyk MA; Izycka-Swieszewska E; Fatyga A; Budka A; Balwierz W; Sobol G; Zalewska-Szewczyk B; Rychlowska-Pruszynska M; Klepacka T; Dembowska-Baginska B; Kazanowska B; Gabrych A; Bien E
[Ad] Endereço:Children's Hospital of Michigan, 3901 Beaubien St, Detroit, MI, USA.
[Ti] Título:Tumor expression of survivin, p53, cyclin D1, osteopontin and fibronectin in predicting the response to neo-adjuvant chemotherapy in children with advanced malignant peripheral nerve sheath tumor.
[So] Source:J Cancer Res Clin Oncol;144(3):519-529, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Selected cell-cycle regulators and extracellular matrix proteins were found to play roles in malignant peripheral nerve sheath tumor (MPNST) biology. We aimed to analyze whether initial tumor tissue expressions of survivin, p53, cyclin D1, osteopontin (OPN) and fibronectin (FN) correlate with the response to neo-adjuvant CHT (naCHT) in children with advanced inoperable MPNST. METHODS: The study included 26 children with MPNST (M/F 14/12, median age 130 months) treated in Polish centers of pediatric oncology between 1992 and 2013. Tissue expression of markers was studied immunohistochemically in the manually performed tissue microarrays and assessed semi-quantitatively as low and high, based on the rate of positive cells and staining intensity. RESULTS: Good response to naCHT was noted in 47.6%, while poor-in 52.4% of patients. The response to naCHT was influenced negatively by the presence of neurofibromatosis NF1 and high initial tumor tissue expression of OPN, survivin, p53 and cyclin D1. Patients with high tumor expression of either OPN, survivin or p53 and those with simultaneous high expression of ≥ 3 of the markers, responded significantly worse to naCHT, than patients, in whom expression of ≤ 2 markers were detected at diagnosis. Nearly, 85% of patients expressing ≥ 3 markers, responded poor to CHT; while 87.5% of children, expressing ≤ 2 markers, were good responders. CONCLUSION: The initial tumor tissue expression of OPN, survivin, p53 and cyclin D1 may serve as markers to predict response to naCHT in pediatric advanced MPNST. Future studies in more numerous group of patients are needed to confirm these preliminary results.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Biomarcadores Tumorais/metabolismo
Ciclina D1/metabolismo
Citocinas/metabolismo
Proteínas Inibidoras de Apoptose/metabolismo
Neoplasias da Bainha Neural/diagnóstico
Neoplasias da Bainha Neural/tratamento farmacológico
Osteopontina/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Biomarcadores Farmacológicos/metabolismo
Criança
Pré-Escolar
Progressão da Doença
Feminino
Seres Humanos
Lactente
Masculino
Terapia Neoadjuvante
Neoplasias da Bainha Neural/metabolismo
Neoplasias da Bainha Neural/patologia
Neurilemoma/tratamento farmacológico
Neurilemoma/metabolismo
Neurilemoma/patologia
Prognóstico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BIRC5 protein, human); 0 (Biomarkers, Pharmacological); 0 (Biomarkers, Tumor); 0 (CCND1 protein, human); 0 (Cytokines); 0 (Inhibitor of Apoptosis Proteins); 0 (SPP1 protein, human); 0 (migration stimulating factor, human); 106441-73-0 (Osteopontin); 136601-57-5 (Cyclin D1)
[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:180115
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-018-2580-1


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[PMID]:29288363
[Au] Autor:Hamurcu Z; Delibasi N; Geçene S; Sener EF; Dönmez-Altuntas H; Özkul Y; Canatan H; Ozpolat B
[Ad] Endereço:Department of Medical Biology, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
[Ti] Título:Targeting LC3 and Beclin-1 autophagy genes suppresses proliferation, survival, migration and invasion by inhibition of Cyclin-D1 and uPAR/Integrin ß1/ Src signaling in triple negative breast cancer cells.
[So] Source:J Cancer Res Clin Oncol;144(3):415-430, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Autophagy is a catabolic process for degrading dysfunctional proteins and organelles, and closely associated with cancer cell survival under therapeutic, metabolic stress, hypoxia, starvation and lack of growth factors, contributing to resistance to therapies. However, the role of autophagy in breast cancer cells is not well understood. In the present study, we investigated the role of autophagy in highly aggressive and metastatic triple negative breast cancer (TNBC) and non-metastatic breast cancer cells and demonstrated that the knockdown of autophagy-related genes (LC3 and Beclin-1) inhibited autophagy and significantly suppressed cell proliferation, colony formation, migration/invasion and induced apoptosis in MDA-MB-231 and BT-549 TNBC cells. Knockdown of LC3 and Beclin-1 led to inhibition of multiple proto-oncogenic signaling pathways, including cyclin D1, uPAR/integrin-ß1/Src, and PARP1. In conclusion, our study suggests that LC3 and Beclin-1 are required for cell proliferation, survival, migration and invasion, and may contribute to tumor growth and progression of highly aggressive and metastatic TNBC cells and therapeutic targeting of autophagy genes may be a potential therapeutic strategy for TNBC in breast cancer.
[Mh] Termos MeSH primário: Beclina-1/antagonistas & inibidores
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Proteínas Associadas aos Microtúbulos/antagonistas & inibidores
Terapia de Alvo Molecular/métodos
RNA Interferente Pequeno/farmacologia
Neoplasias de Mama Triplo Negativas/patologia
[Mh] Termos MeSH secundário: Autofagia/genética
Beclina-1/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Ciclina D1/antagonistas & inibidores
Ciclina D1/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Integrina beta1/metabolismo
Células MCF-7
Proteínas Associadas aos Microtúbulos/genética
Receptores de Ativador de Plasminogênio Tipo Uroquinase/antagonistas & inibidores
Receptores de Ativador de Plasminogênio Tipo Uroquinase/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
Neoplasias de Mama Triplo Negativas/genética
Quinases da Família src/antagonistas & inibidores
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Beclin-1); 0 (CCND1 protein, human); 0 (Integrin beta1); 0 (Microtubule-Associated Proteins); 0 (RNA, Small Interfering); 0 (Receptors, Urokinase Plasminogen Activator); 0 (light chain 3, human); 136601-57-5 (Cyclin D1); EC 2.7.10.2 (src-Family Kinases)
[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:171231
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2557-5


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[PMID]:27776340
[Au] Autor:Liang L; Yang X; Yu Y; Li X; Wu Y; Shi R; Jiang J; Gao L; Ye F; Zhao Q; Li R; Wei L; Han Z
[Ad] Endereço:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, the Second Military Medical University, Shanghai, China.
[Ti] Título:Babao Dan attenuates hepatic fibrosis by inhibiting hepatic stellate cells activation and proliferation via TLR4 signaling pathway.
[So] Source:Oncotarget;7(50):82554-82566, 2016 Dec 13.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Babao Dan (BBD), a traditional Chinese medicine, has been widely used as a complementary and alternative medicine to treat chronic liver diseases. In this study, we aimed to observe the protective effect of BBD on rat hepatic fibrosis induced by diethylnitrosamine (DEN) and explore it possible mechanism. BBD was administrated while DEN was given. After eight weeks, values of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) indicated that BBD significantly protected liver from damaging by DEN and had no obvious side effect on normal rat livers. Meanwhile, BBD attenuated hepatic inflammation and fibrosis in DEN-induced rat livers through histopathological examination and hepatic hydroxyproline content. Furthermore, we found that BBD inhibited hepatic stellate cells activation and proliferation without altering the concentration of lipopolysaccharide (LPS) in portal vein. In vitro study, serum from BBD treated rats (BBD-serum) could also significantly suppress LPS-induced HSCs activation through TLR4/NF-κB pathway. In addition, BBD-serum also inhibited the proliferation of HSCs by regulating TLR4/ERK pathway. Our study demonstrated that BBD may provide a new therapy strategy of hepatic injury and hepatic fibrosis.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Medicamentos de Ervas Chinesas/farmacologia
Células Estreladas do Fígado/efeitos dos fármacos
Cirrose Hepática Experimental/prevenção & controle
Fígado/efeitos dos fármacos
Substâncias Protetoras/farmacologia
Transdução de Sinais/efeitos dos fármacos
Receptor 4 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Animais
Doença Hepática Induzida por Substâncias e Drogas/metabolismo
Doença Hepática Induzida por Substâncias e Drogas/patologia
Ciclina D1/metabolismo
Citocinas/metabolismo
Citoproteção
Dietilnitrosamina
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Células Estreladas do Fígado/metabolismo
Células Estreladas do Fígado/patologia
Lipopolissacarídeos/farmacologia
Fígado/metabolismo
Fígado/patologia
Cirrose Hepática Experimental/induzido quimicamente
Cirrose Hepática Experimental/metabolismo
Cirrose Hepática Experimental/patologia
Masculino
NF-kappa B/metabolismo
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccnd1 protein, rat); 0 (Cytokines); 0 (Drugs, Chinese Herbal); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Protective Agents); 0 (Tlr4 protein, rat); 0 (Toll-Like Receptor 4); 136601-57-5 (Cyclin D1); 3IQ78TTX1A (Diethylnitrosamine); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[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:161025
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.12783


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[PMID]:29351283
[Au] Autor:Sun G; SiMa G; Wu C; Fan Y; Tan Y; Wang Z; Cheng G; Li J
[Ad] Endereço:Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou Shi, China.
[Ti] Título:Decreased MiR-17 in glioma cells increased cell viability and migration by increasing the expression of Cyclin D1, p-Akt and Akt.
[So] Source:PLoS One;13(1):e0190515, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The activating mutations of micro RNA (miR)-17 have been revealed in tumors such as human non-Hodgkin's lymphoma and T cell leukemia. However, it is unclear about the role of miR-17 in glioma cells. The current study aimed to investigate effects of miR-17 mimics or inhibitor on the viability and migration of rat glioma C6 cells, and explore possible mechanisms. METHODS: The expression of miR-17 in rat glioma C6 cells and normal brain tissue was detected by quantitative PCR. Protein expression of Cyclin D1 in rat glioma C6 cells and normal brain tissue was measured by Western Blot. Glioma C6 cells were transfected with MiR-17 mimics or inhibitor. Cells that were not transfected (Lipofectamine only) and cells that were transfected with nonsense RNA negative control served as control. MTT assay was utilized to detect cell viability, and cell wound scratch assay was utilized to examine the migration index. In addition, protein expression of Cyclin D1, p-Akt and Akt in MiR-17 mimics or inhibitor-transfected glioma C6 cells was detected by Western Blot. This study had been approved by the Medical Ethics Committee of the First Affiliated Hospital of Soochow University. All applicable international, national, and/or institutional guidelines for the care and use of animals were followed. RESULTS: The expression of miR-17 was significantly lower, whereas the expression of Cyclin D1 was significantly higher in glioma C6 cells compared to normal brain tissue. MiR-17 mimics decreased the viability and migration of glioma C6 cells markedly at 48 h. In addition, MiR-17 inhibitor increased the viability and migration of glioma C6 cells at 24 and 48 h. The protein expression of Cyclin D1, p-Akt and Akt in glioma C6 cells decreased after transfection with miR-17 mimics for 72 h, and increased after transfection with miR-17 inhibitor for 72 h. CONCLUSIONS: The reduced miR-17 levels in glioma cells increased cell viability and migration, which correlates with increased expression of Cyclin D1, p-Akt and Akt.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/metabolismo
Movimento Celular/genética
Sobrevivência Celular/genética
Ciclina D1/genética
Glioma/metabolismo
MicroRNAs/metabolismo
Proteínas Proto-Oncogênicas c-akt/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Masculino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccnd1 protein, rat); 0 (MIRN17 microRNA, rat); 0 (MicroRNAs); 136601-57-5 (Cyclin D1); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190515


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[PMID]:29198702
[Au] Autor:Wu D; Liang M; Dang H; Fang F; Xu F; Liu C
[Ad] Endereço:Department of Pediatric Intensive Care Unit, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongq
[Ti] Título:Hydrogen protects against hyperoxia-induced apoptosis in type II alveolar epithelial cells via activation of PI3K/Akt/Foxo3a signaling pathway.
[So] Source:Biochem Biophys Res Commun;495(2):1620-1627, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxidative stress is regarded as a key regulator in the pathogenesis of prolonged hyperoxia-induced lung injury, which causes injury to alveolar epithelial cells and eventually leads to development of bronchopulmonary dysplasia (BPD). Many studies have shown that hydrogen has a protective effect in a variety of cells. However, the mechanisms by which hydrogen rescues cells from damage due to oxidative stress in BPD remains to be fully elucidated. This study sought to evaluate the effects of hydrogen on hyperoxia-induced lung injury and to investigate the underlying mechanism. Primary type II alveolar epithelial cells (AECIIs) were divided into four groups: control (21% oxygen), hyperoxia (95% oxygen), hyperoxia + hydrogen, and hyperoxia + hydrogen + LY294002 (a PI3K/Akt inhibitor). Proliferation and apoptosis of AECIIs were assessed using MTS assay and flow cytometry (FCM), respectively. Gene and protein expression were detected by quantitative polymerase chain reaction (q-PCR) and western blot analysis. Stimulation with hyperoxia decreased the expression of P-Akt, P- FoxO3a, cyclinD1 and Bcl-2. Hyperoxic conditions increased levels of Bim, Bax, and Foxo3a, which induced proliferation restriction and apoptosis of AECIIs. These effects of hyperoxia were reversed with hydrogen pretreatment. Furthermore, the protective effects of hydrogen were abrogated by PI3K/Akt inhibitor LY294002. The results indicate that hydrogen protects AECIIs from hyperoxia-induced apoptosis by inhibiting apoptosis factors and promoting the expression of anti-apoptosis factors. These effects were associated with activation of the PI3K/Akt/FoxO3a pathway.
[Mh] Termos MeSH primário: Células Epiteliais Alveolares/efeitos dos fármacos
Células Epiteliais Alveolares/metabolismo
Hidrogênio/farmacologia
Hiperóxia/tratamento farmacológico
Hiperóxia/metabolismo
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/tratamento farmacológico
Lesão Pulmonar Aguda/metabolismo
Lesão Pulmonar Aguda/patologia
Células Epiteliais Alveolares/patologia
Animais
Apoptose/efeitos dos fármacos
Proteína 11 Semelhante a Bcl-2/genética
Células Cultivadas
Ciclina D1/genética
Feminino
Proteína Forkhead Box O3/genética
Proteína Forkhead Box O3/metabolismo
Expressão Gênica/efeitos dos fármacos
Genes bcl-2/efeitos dos fármacos
Hidrogênio/metabolismo
Hiperóxia/patologia
Estresse Oxidativo/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/metabolismo
Gravidez
Proteínas Proto-Oncogênicas c-akt/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Proteína X Associada a bcl-2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bax protein, rat); 0 (Bcl-2-Like Protein 11); 0 (Bcl2l11 protein, rat); 0 (Ccnd1 protein, rat); 0 (Forkhead Box Protein O3); 0 (Foxo3a protein, rat); 0 (RNA, Messenger); 0 (bcl-2-Associated X Protein); 136601-57-5 (Cyclin D1); 7YNJ3PO35Z (Hydrogen); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[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:171205
[St] Status:MEDLINE



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