Base de dados : MEDLINE
Pesquisa : D12.644.360.262.180 [Categoria DeCS]
Referências encontradas : 2541 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 255 ir para página                         

  1 / 2541 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28460453
[Au] Autor:Yu T; Wu Y; Hu Q; Zhang J; Nie E; Wu W; Wang X; Wang Y; Liu N
[Ad] Endereço:Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
[Ti] Título:CBX7 is a glioma prognostic marker and induces G1/S arrest via the silencing of CCNE1.
[So] Source:Oncotarget;8(16):26637-26647, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chromobox homolog 7 (CBX7) cooperates with other polycomb group (PcG) proteins to maintain target genes in a silenced state. However, the precise role of CBX7 in tumor progression is still controversial. We found that the expression of CBX7 in four public databases was significantly lower in high grade glioma (HGG). The reduced expression of CBX7 correlated with poor outcome in HGG patients. Both KEGG and GO analyses indicated that genes that were negatively correlated to CBX7 were strongly associated with the cell cycle pathway. We observed that decreased CBX7 protein levels enhanced glioma cells proliferation, migration and invasion. Then, we verified that CBX7 overexpression arrested cells in the G0/G1 phase. Moreover, we demonstrated that the underlying mechanism involved in CBX7 induced repression of CCNE1 promoter requiring the recruitment of histone deacetylase 2 (HADC2). Finally, in vivo bioluminescence imaging and survival times of nude mice revealed that CBX7 behaved as a tumor suppressor in gliomas. In summary, our results validate the assumption that CBX7 is a tumor suppressor of gliomas. Moreover, CBX7 is a potential and novel prognostic biomarker in glioma patients. We also clarified that CBX7 silences CCNE1 via the combination of CCNE1 promoter and the recruitment of HDAC2.
[Mh] Termos MeSH primário: Ciclina E/genética
Pontos de Checagem da Fase G1 do Ciclo Celular/genética
Inativação Gênica
Glioma/genética
Glioma/mortalidade
Proteínas Oncogênicas/genética
Complexo Repressor Polycomb 1/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Modelos Animais de Doenças
Feminino
Regulação Neoplásica da Expressão Gênica
Glioma/patologia
Xenoenxertos
Histona Desacetilase 2/metabolismo
Seres Humanos
Masculino
Camundongos
Gradação de Tumores
Complexo Repressor Polycomb 1/metabolismo
Prognóstico
Regiões Promotoras Genéticas
Ligação Proteica
RNA Interferente Pequeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CBX7 protein, human); 0 (CCNE1 protein, human); 0 (Cyclin E); 0 (Oncogene Proteins); 0 (RNA, Small Interfering); EC 2.3.2.27 (Polycomb Repressive Complex 1); EC 3.5.1.98 (Histone Deacetylase 2)
[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.15789


  2 / 2541 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29326043
[Au] Autor:Zhang Z; Shen M; Zhou G
[Ad] Endereço:Department of Gastrointestinal Surgery, Huai'an First People's Hospital, Affiliated to Nanjing Medical University, Huai'an City, Jiangsu Province, PR China.
[Ti] Título:Upregulation of CDCA5 promotes gastric cancer malignant progression via influencing cyclin E1.
[So] Source:Biochem Biophys Res Commun;496(2):482-489, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cell division cycle associated 5(CDCA5) was reported to be associated with progression of several human cancers, however, its clinical significance and biological role still remain unknown in gastric cancer(GC). By analyzing The Cancer Genome Atlas(TCGA), we found CDCA5 was significantly upregulated in GC tissues compared to adjacent normal tissues. Tissue microarray(TMA) indicated upregulation of CDCA5 was significantly correlated with more advanced clinicopathological features, and acts as an independent risk factor for worse overall survival(OS) in GC patients. Moreover, silence of CDCA5 suppresses proliferation of GC cells by inducing G1-phase arrest via downregulating Cyclin E1(CCNE1). Our results demonstrate upregulation of CDCA5 promotes GC malignant progression, which may offer a potential prognostic and therapeutic strategy.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/genética
Adenocarcinoma/genética
Proteínas de Ciclo Celular/genética
Ciclina E/genética
Regulação Neoplásica da Expressão Gênica
Proteínas Oncogênicas/genética
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Adenocarcinoma/diagnóstico
Adenocarcinoma/metabolismo
Adenocarcinoma/mortalidade
Idoso
Animais
Proteínas de Ciclo Celular/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Ciclina E/metabolismo
Feminino
Pontos de Checagem da Fase G1 do Ciclo Celular/genética
Perfilação da Expressão Gênica
Seres Humanos
Masculino
Camundongos
Camundongos Nus
Meia-Idade
Transplante de Neoplasias
Proteínas Oncogênicas/metabolismo
Prognóstico
Transdução de Sinais
Neoplasias Gástricas/diagnóstico
Neoplasias Gástricas/metabolismo
Neoplasias Gástricas/mortalidade
Análise de Sobrevida
Análise Serial de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (CCNE1 protein, human); 0 (CDCA5 protein, human); 0 (Cell Cycle Proteins); 0 (Cyclin E); 0 (Oncogene Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE


  3 / 2541 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28993193
[Au] Autor:Yang L; Wen Y; Lv G; Lin Y; Tang J; Lu J; Zhang M; Liu W; Sun X
[Ad] Endereço:Shenzhen Tumor Immuno-gene Therapy Clinical Application Engineering Lab, Biobank of Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen 518035, PR China; Institute of Immunology of Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510060, G
[Ti] Título:α-Lipoic acid inhibits human lung cancer cell proliferation through Grb2-mediated EGFR downregulation.
[So] Source:Biochem Biophys Res Commun;494(1-2):325-331, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Alpha lipoic acid (α -LA) is a naturally occurring antioxidant and metabolic enzyme co-factor. Recently, α -LA has been reported to inhibit the growth of various cancer cells, but the precise signaling pathways that mediate the effects of α -LA on non-small cell lung cancer (NSCLC) development remain unclear. METHODS: The CCK-8 assay was used to assess cell proliferation in NSCLC cell lines after α -LA treatment. The expression of growth factor receptor-bound protein 2 (Grb2), cyclin-dependent kinase (CDK)-2, CDK4, CDK6, Cyclin D3, Cyclin E1, Ras, c-Raf, epidermal growth factor receptor (EGFR), ERK1/2 and activated EGFR and ERK1/2 was evaluated by western blotting. Grb2 levels were restored in α-LA-treated cells by transfection of a plasmid carrying Grb2 and were reduced in NSCLC cells via specific siRNA-mediated knockdown. RESULTS: α -LA dramatically decreased NSCLC cell proliferation by downregulating Grb2; in contrast, Grb2 overexpression significantly prevented α-LA-induced decrease in cell growth in vitro. Western blot analysis indicated that α-LA decreased the levels of phospho-EGFR, CDK2/4/6, Cyclins D3 and E1, which are associated with the inhibition of G1/S-phase transition. Additional experiments indicated that Grb2 inhibition partially abolished EGF-induced phospho-EGFR and phospho-ERK1/2 activity. In addition, α-LA exerted greater inhibitory effects than gefitinib on NSCLC cells by preventing EGF-induced EGFR activation. CONCLUSION: For the first time, these findings provide the first evidence that α-LA inhibits cell proliferation through Grb2 by suppressing EGFR phosphorylation and that MAPK/ERK is involved in this pathway.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Proteína Adaptadora GRB2/antagonistas & inibidores
Regulação Neoplásica da Expressão Gênica
Ácido Tióctico/farmacologia
[Mh] Termos MeSH secundário: Células A549
Proliferação Celular/efeitos dos fármacos
Ciclina D3/genética
Ciclina D3/metabolismo
Ciclina E/genética
Ciclina E/metabolismo
Quinase 2 Dependente de Ciclina/genética
Quinase 2 Dependente de Ciclina/metabolismo
Quinase 4 Dependente de Ciclina/genética
Quinase 4 Dependente de Ciclina/metabolismo
Quinase 6 Dependente de Ciclina/genética
Quinase 6 Dependente de Ciclina/metabolismo
Proteína Adaptadora GRB2/genética
Proteína Adaptadora GRB2/metabolismo
Seres Humanos
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Proteínas Oncogênicas/genética
Proteínas Oncogênicas/metabolismo
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-raf/genética
Proteínas Proto-Oncogênicas c-raf/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Receptor do Fator de Crescimento Epidérmico/genética
Receptor do Fator de Crescimento Epidérmico/metabolismo
Transdução de Sinais
Proteínas ras/genética
Proteínas ras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CCND3 protein, human); 0 (CCNE1 protein, human); 0 (Cyclin D3); 0 (Cyclin E); 0 (GRB2 Adaptor Protein); 0 (GRB2 protein, human); 0 (Oncogene Proteins); 0 (RNA, Small Interfering); 73Y7P0K73Y (Thioctic Acid); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.1 (Proto-Oncogene Proteins c-raf); EC 2.7.11.22 (CDK2 protein, human); EC 2.7.11.22 (CDK4 protein, human); EC 2.7.11.22 (CDK6 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 2); EC 2.7.11.22 (Cyclin-Dependent Kinase 4); EC 2.7.11.22 (Cyclin-Dependent Kinase 6); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE


  4 / 2541 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28797035
[Au] Autor:Zagouri F; Kotoula V; Kouvatseas G; Sotiropoulou M; Koletsa T; Gavressea T; Valavanis C; Trihia H; Bobos M; Lazaridis G; Koutras A; Pentheroudakis G; Skarlos P; Bafaloukos D; Arnogiannaki N; Chrisafi S; Christodoulou C; Papakostas P; Aravantinos G; Kosmidis P; Karanikiotis C; Zografos G; Papadimitriou C; Fountzilas G
[Ad] Endereço:Department of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens School of Medicine, Athens, Greece.
[Ti] Título:Protein expression patterns of cell cycle regulators in operable breast cancer.
[So] Source:PLoS One;12(8):e0180489, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND-AIM: To evaluate the prognostic role of elaborate molecular clusters encompassing cyclin D1, cyclin E1, p21, p27 and p53 in the context of various breast cancer subtypes. METHODS: Cyclin E1, cyclin D1, p53, p21 and p27 were evaluated with immunohistochemistry in 1077 formalin-fixed paraffin-embedded tissues from breast cancer patients who had been treated within clinical trials. Jaccard distances were computed for the markers and the resulted matrix was used for conducting unsupervised hierarchical clustering, in order to identify distinct groups correlating with prognosis. RESULTS: Luminal B and triple-negative (TNBC) tumors presented with the highest and lowest levels of cyclin D1 expression, respectively. By contrast, TNBC frequently expressed Cyclin E1, whereas ER-positive tumors did not. Absence of Cyclin D1 predicted for worse OS, while absence of Cyclin E1 for poorer DFS. The expression patterns of all examined proteins yielded 3 distinct clusters; (1) Cyclin D1 and/or E1 positive with moderate p21 expression; (2) Cyclin D1 and/or E1, and p27 positive, p53 protein negative; and, (3) Cyclin D1 or E1 positive, p53 positive, p21 and p27 negative or moderately positive. The 5-year DFS rates for clusters 1, 2 and 3 were 70.0%, 79.1%, 67.4% and OS 88.4%, 90.4%, 78.9%, respectively. CONCLUSIONS: It seems that the expression of cell cycle regulators in the absence of p53 protein is associated with favorable prognosis in operable breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Mama/patologia
Ciclina D1/análise
Ciclina E/análise
Inibidor de Quinase Dependente de Ciclina p21/análise
Inibidor de Quinase Dependente de Ciclina p27/análise
Proteínas Oncogênicas/análise
Proteína Supressora de Tumor p53/análise
[Mh] Termos MeSH secundário: Adulto
Idoso
Antineoplásicos/uso terapêutico
Mama/efeitos dos fármacos
Neoplasias da Mama/diagnóstico
Neoplasias da Mama/tratamento farmacológico
Feminino
Seres Humanos
Imuno-Histoquímica
Meia-Idade
Prognóstico
Análise de Sobrevida
Neoplasias de Mama Triplo Negativas/diagnóstico
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
Neoplasias de Mama Triplo Negativas/patologia
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CCND1 protein, human); 0 (CCNE1 protein, human); 0 (CDKN1A protein, human); 0 (Cyclin E); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (Oncogene Proteins); 0 (Tumor Suppressor Protein p53); 136601-57-5 (Cyclin D1); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180489


  5 / 2541 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28760857
[Au] Autor:Takada M; Zhang W; Suzuki A; Kuroda TS; Yu Z; Inuzuka H; Gao D; Wan L; Zhuang M; Hu L; Zhai B; Fry CJ; Bloom K; Li G; Karpen GH; Wei W; Zhang Q
[Ad] Endereço:Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina.
[Ti] Título:FBW7 Loss Promotes Chromosomal Instability and Tumorigenesis via Cyclin E1/CDK2-Mediated Phosphorylation of CENP-A.
[So] Source:Cancer Res;77(18):4881-4893, 2017 Sep 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The centromere regulates proper chromosome segregation, and its dysfunction is implicated in chromosomal instability (CIN). However, relatively little is known about how centromere dysfunction occurs in cancer. Here, we define the consequences of phosphorylation by cyclin E1/CDK2 on a conserved Ser18 residue of centromere-associated protein CENP-A, an essential histone H3 variant that specifies centromere identity. Ser18 hyperphosphorylation in cells occurred upon loss of FBW7, a tumor suppressor whose inactivation leads to CIN. This event on CENP-A reduced its centromeric localization, increased CIN, and promoted anchorage-independent growth and xenograft tumor formation. Overall, our results revealed a pathway that cyclin E1/CDK2 activation coupled with FBW7 loss promotes CIN and tumor progression via CENP-A-mediated centromere dysfunction. .
[Mh] Termos MeSH primário: Autoantígenos/metabolismo
Neoplasias da Mama/patologia
Proteínas de Ciclo Celular/metabolismo
Transformação Celular Neoplásica/patologia
Instabilidade Cromossômica
Proteínas Cromossômicas não Histona/metabolismo
Neoplasias do Colo/patologia
Ciclina E/metabolismo
Quinase 2 Dependente de Ciclina/metabolismo
Proteínas F-Box/metabolismo
Proteínas Oncogênicas/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Apoptose
Biomarcadores Tumorais/metabolismo
Neoplasias da Mama/genética
Neoplasias da Mama/metabolismo
Ciclo Celular
Proliferação Celular
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Centrômero
Proteína Centromérica A
Neoplasias do Colo/genética
Neoplasias do Colo/metabolismo
Proteína 7 com Repetições F-Box-WD
Feminino
Histonas/metabolismo
Seres Humanos
Fosforilação
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantigens); 0 (Biomarkers, Tumor); 0 (CCNE1 protein, human); 0 (CENPA protein, human); 0 (Cell Cycle Proteins); 0 (Centromere Protein A); 0 (Chromosomal Proteins, Non-Histone); 0 (Cyclin E); 0 (F-Box Proteins); 0 (F-Box-WD Repeat-Containing Protein 7); 0 (FBXW7 protein, human); 0 (Histones); 0 (Oncogene Proteins); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.22 (CDK2 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-17-1240


  6 / 2541 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28628119
[Au] Autor:Tian R; Wang J; Yan H; Wu J; Xu Q; Zhan X; Gui Z; Ding M; He J
[Ad] Endereço:Department of Pathology, Anhui Provincial Hospital affiliated to Anhui Medical University and Anhui Provincial Cancer Hospital, Hefei, China.
[Ti] Título:Differential expression of miR16 in glioblastoma and glioblastoma stem cells: their correlation with proliferation, differentiation, metastasis and prognosis.
[So] Source:Oncogene;36(42):5861-5873, 2017 Oct 19.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The function of miR16 in multiforme glioblastoma multiforme (GBM) and its stem cells (GSCs) remains elusive. To this end, we investigated the patterns of miR16 expression in these cells and their correlation with malignant behaviors and clinical outcomes. The levels of miR16 and its targeted genes in tumor tissue of GBM and GBM SGH44, U87, U251 cells as well as their stem cell counterparts were measured by qRT-PCR or western blot or immunohistochemistry. Luciferase reporter assay was used to confirm the binding of miR16 to 3'-UTR of its target genes. The effects of miR16 on malignant behaviors were investigated, including tumor cell viability, soft-agar colony formation, GSCs Matrigel colony forming and migration and invasion as well as nude mice xenograft model. Differentially expression patterns of miR16 in glioblastoma cells and GSCs cells were found in this study. Changes of miR16 targeted genes, Bcl2 (B cell lymphoma 2), CDK6 (Cyclin-dependent kinase 6), CCND1 (cyclin D1), CCNE1 (cyclin E1) and SOX5 were confirmed in glioblastoma cell lines and tissue specimens. In vitro and in vivo studies showed that tumor cell proliferation was inhibited by miR16 mimic, but enhanced by miR16 inhibitor. The expression level of miR16 positively correlates with GSCs differentiation, but negatively with the abilities of migration, motility, invasion and colony formation in glioblastoma cells. The inhibitory effects of miR16 on its target genes were also found in nude mice xenograft model. Our findings revealed that the miR16 functions as a tumor suppressor in GSCs and its association with prognosis in GBM.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Neoplasias Encefálicas/patologia
Glioblastoma/genética
Glioblastoma/patologia
MicroRNAs/genética
Células-Tronco Neoplásicas/patologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Animais
Encéfalo/metabolismo
Neoplasias Encefálicas/genética
Neoplasias Encefálicas/metabolismo
Estudos de Casos e Controles
Diferenciação Celular
Linhagem Celular Tumoral
Proliferação Celular
Criança
Ciclina D1/metabolismo
Ciclina E/metabolismo
Quinase 6 Dependente de Ciclina/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica
Glioblastoma/metabolismo
Seres Humanos
Masculino
Camundongos
Camundongos Nus
Meia-Idade
Células-Tronco Neoplásicas/metabolismo
Proteínas Oncogênicas/metabolismo
Prognóstico
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Fatores de Transcrição SOXD/metabolismo
Taxa de Sobrevida
Ensaios Antitumorais Modelo de Xenoenxerto
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCL2 protein, human); 0 (Biomarkers, Tumor); 0 (CCND1 protein, human); 0 (CCNE1 protein, human); 0 (Cyclin E); 0 (MIRN16 microRNA, human); 0 (MicroRNAs); 0 (Oncogene Proteins); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (SOX5 protein, human); 0 (SOXD Transcription Factors); 136601-57-5 (Cyclin D1); EC 2.7.11.22 (CDK6 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 6)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.182


  7 / 2541 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28618963
[Au] Autor:Zhang X; Zhang Y; Fan C; Wang L; Liu Y; Li A; Jiang G; Zhou H; Cai L; Miao Y
[Ad] Endereço:1 Department of Pathology, The First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, China.
[Ti] Título:Noxin promotes proliferation of breast cancer cells via P38-ATF2 signaling pathway.
[So] Source:Tumour Biol;39(6):1010428317705515, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Noxin (also called chromosome 11 open reading frame 82 or DNA damage-induced apoptosis suppressor) is associated with anti-apoptosis and cell proliferation in response to stress signals. However, to our knowledge, the role of Noxin in regulating cell proliferation is still controversial and there are no reports of the function and clinicopathological association in breast cancer. In this study, immunohistochemistry results showed that Noxin expression was significantly correlated with advanced tumor-node-metastasis stage ( p = 0.027), positive regional lymph node metastasis ( p = 0.002), and poor overall survival ( p = 0.002). Proliferation assay results showed that Noxin obviously promoted the ability of proliferation of normal breast cells. Subsequent western blot results revealed that Cyclin D1 and Cyclin E1 were upregulated by overexpressing Noxin, whereas Cyclin D1 and Cyclin E1 were downregulated after depleting Noxin. The levels of phosphorylated P38 and activating transcription factor 2 were obviously increased after overexpressing Noxin, and their expression was downregulated accordingly by transfecting Noxin-small interfering RNA. Moreover, P38 inhibitor counteracted the elevating expression of phosphorylated activating transcription factor 2, Cyclin D1, and Cyclin E1 induced by Noxin overexpression and thereby reversed the effect of Noxin overexpression on facilitating cell growth. Taken together, our studies indicated that Noxin was overexpressed in breast cancer and its positive expression was significantly correlated with advance tumor-node-metastasis stage, positive lymph node metastasis, and poor prognosis. Noxin facilitated the expression of Cyclin D1 and Cyclin E1 through activating P38-activating transcription factor 2 signaling pathway, thus enhanced cell growth of breast cancer.
[Mh] Termos MeSH primário: Fator 2 Ativador da Transcrição/genética
Proteínas Reguladoras de Apoptose/genética
Neoplasias da Mama/genética
Ciclina D1/biossíntese
Ciclina E/biossíntese
Proteínas Oncogênicas/biossíntese
Proteínas Quinases p38 Ativadas por Mitógeno/genética
[Mh] Termos MeSH secundário: Fator 2 Ativador da Transcrição/biossíntese
Adulto
Apoptose/genética
Neoplasias da Mama/patologia
Neoplasias da Mama/terapia
Ciclo Celular/genética
Proliferação Celular/genética
Ciclina D1/genética
Ciclina E/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Metástase Linfática
Células MCF-7
Meia-Idade
Estadiamento de Neoplasias
Proteínas Oncogênicas/genética
RNA Interferente Pequeno/genética
Transdução de Sinais/genética
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATF2 protein, human); 0 (Activating Transcription Factor 2); 0 (Apoptosis Regulatory Proteins); 0 (CCNE1 protein, human); 0 (Cyclin E); 0 (Oncogene Proteins); 0 (RNA, Small Interfering); 0 (noxin protein, human); 136601-57-5 (Cyclin D1); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317705515


  8 / 2541 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28582471
[Au] Autor:Brun S; Abella N; Berciano MT; Tapia O; Jaumot M; Freire R; Lafarga M; Agell N
[Ad] Endereço:Departament Biomedicina, Universitat de Barcelona, IDIBAPS, Barcelona, Spain.
[Ti] Título:SUMO regulates p21Cip1 intracellular distribution and with p21Cip1 facilitates multiprotein complex formation in the nucleolus upon DNA damage.
[So] Source:PLoS One;12(6):e0178925, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously showed that p21Cip1 transits through the nucleolus on its way from the nucleus to the cytoplasm and that DNA damage inhibits this transit and induces the formation of p21Cip1-containing intranucleolar bodies (INoBs). Here, we demonstrate that these INoBs also contain SUMO-1 and UBC9, the E2 SUMO-conjugating enzyme. Furthermore, whereas wild type SUMO-1 localized in INoBs, a SUMO-1 mutant, which is unable to conjugate with proteins, does not, suggesting the presence of SUMOylated proteins at INoBs. Moreover, depletion of the SUMO-conjugating enzyme UBC9 or the sumo hydrolase SENP2 changed p21Cip1 intracellular distribution. In addition to SUMO-1 and p21Cip1, cell cycle regulators and DNA damage checkpoint proteins, including Cdk2, Cyclin E, PCNA, p53 and Mdm2, and PML were also detected in INoBs. Importantly, depletion of UBC9 or p21Cip1 impacted INoB biogenesis and the nucleolar accumulation of the cell cycle regulators and DNA damage checkpoint proteins following DNA damage. The impact of p21Cip1 and SUMO-1 on the accumulation of proteins in INoBs extends also to CRM1, a nuclear exportin that is also important for protein translocation from the cytoplasm to the nucleolus. Thus, SUMO and p21Cip1 regulate the transit of proteins through the nucleolus, and that disruption of nucleolar export by DNA damage induces SUMO and p21Cip1 to act as hub proteins to form a multiprotein complex in the nucleolus.
[Mh] Termos MeSH primário: Nucléolo Celular/metabolismo
Inibidor de Quinase Dependente de Ciclina p21/genética
Regulação da Expressão Gênica
Organelas/metabolismo
Proteína SUMO-1/metabolismo
[Mh] Termos MeSH secundário: Nucléolo Celular/genética
Ciclina E/genética
Ciclina E/metabolismo
Quinase 2 Dependente de Ciclina/genética
Quinase 2 Dependente de Ciclina/metabolismo
Inibidor de Quinase Dependente de Ciclina p21/deficiência
Cisteína Endopeptidases/genética
Cisteína Endopeptidases/metabolismo
Dano ao DNA
Células HCT116
Seres Humanos
Carioferinas/genética
Carioferinas/metabolismo
Biogênese de Organelas
Organelas/genética
Antígeno Nuclear de Célula em Proliferação/genética
Antígeno Nuclear de Célula em Proliferação/metabolismo
Proteína da Leucemia Promielocítica/genética
Proteína da Leucemia Promielocítica/metabolismo
Ligação Proteica
Multimerização Proteica
Transporte Proteico
Proteínas Proto-Oncogênicas c-mdm2/genética
Proteínas Proto-Oncogênicas c-mdm2/metabolismo
Receptores Citoplasmáticos e Nucleares/genética
Receptores Citoplasmáticos e Nucleares/metabolismo
Proteína SUMO-1/genética
Transdução de Sinais
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
Enzimas de Conjugação de Ubiquitina/deficiência
Enzimas de Conjugação de Ubiquitina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN1A protein, human); 0 (Cyclin E); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (Karyopherins); 0 (Proliferating Cell Nuclear Antigen); 0 (Promyelocytic Leukemia Protein); 0 (Receptors, Cytoplasmic and Nuclear); 0 (SUMO-1 Protein); 0 (SUMO1 protein, human); 0 (Tumor Suppressor Protein p53); 0 (exportin 1 protein); 143220-95-5 (PML protein, human); EC 2.3.2.23 (Ubiquitin-Conjugating Enzymes); EC 2.3.2.27 (MDM2 protein, human); EC 2.3.2.27 (Proto-Oncogene Proteins c-mdm2); EC 2.7.11.22 (CDK2 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 2); EC 3.4.22.- (Cysteine Endopeptidases); EC 3.4.22.- (SENP2 protein, human); EC 6.3.2.- (ubiquitin-conjugating enzyme UBC9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178925


  9 / 2541 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28581882
[Au] Autor:Park YM; Kim MA; Jung HT; Kang HJ; Yoo HS; Kang IC
[Ad] Endereço:1 Department of Biological Science, College of Life and Health Sciences, Hoseo University , Asan, Korea.
[Ti] Título:Nutriproteomic Analysis of Hwangmaemok-Induced Antiangiogenic Effect Using Antibody-Arrayed Protein Chip Assay.
[So] Source:J Med Food;20(6):586-591, 2017 Jun.
[Is] ISSN:1557-7600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We investigated the antiangiogenic effects of Lindera obtusiloba Blume (Hwangmaemok, HMM), which is a plant in the Lauraceae family that is commonly used to treat colds and gastritis. Moreover, given that a recent study reported the inhibitory effects of HMM extract on cancer metastasis, we hypothesized that HMM extract might possess and antiangiogenic function. Thus, this study was conducted to investigate the effects of HMM extract on endothelial cell proliferation, migration, and neovascularization in chick chorioallantoic membrane (CAM), and investigated the molecular mechanism of antiangiogenesis using a ProteoChip-based proteomics technology. To examine the effects of HMM extracts on endothelial cell proliferation and migration, we conducted basic fibroblast growth factor (bFGF)-induced human umbilical vein endothelial cell (HUVEC) proliferation and migration. To assess the molecular mechanism of the antiangiogenic effects of HMM extract, a ProteoChip-based forwarded phase antibody array was employed to identify the differential expression of cell cycle proteins in HMM-treated HUVECs. HMM extract inhibited bFGF-induced HUVEC proliferation and migration in a dose-dependent manner and CAM angiogenesis. The ProteoChip-based antibody microarray data showed upregulation of Nibrin/NBS1 and downregulation of Plk-1 and Cyclin E, which are involved in cell division and controlling the cell cycle in bFGF-induced HUVECs. These data suggest that HMM may be a potent antitumor medicinal herb. The present study demonstrates that the antiangiogenic effect of HMM may be due to suppression of endothelial cell proliferation and migration. Taken together, these results emphasize the potential to use HMM extract as a potent angiogenesis inhibitor to treat cancer.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/farmacologia
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Lindera/química
Extratos Vegetais/farmacologia
[Mh] Termos MeSH secundário: Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Ciclina E/genética
Ciclina E/metabolismo
Células Endoteliais da Veia Umbilical Humana/química
Células Endoteliais da Veia Umbilical Humana/citologia
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Análise Serial de Proteínas
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
Proteômica
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Cell Cycle Proteins); 0 (Cyclin E); 0 (Plant Extracts); 0 (Proto-Oncogene Proteins); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (polo-like kinase 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1089/jmf.2016.3775


  10 / 2541 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28520165
[Au] Autor:Bangen JM; Hammerich L; Sonntag R; Baues M; Haas U; Lambertz D; Longerich T; Lammers T; Tacke F; Trautwein C; Liedtke C
[Ad] Endereço:Department of Internal Medicine III, RWTH Aachen University, Aachen, Germany.
[Ti] Título:Targeting CCl -induced liver fibrosis by RNA interference-mediated inhibition of cyclin E1 in mice.
[So] Source:Hepatology;66(4):1242-1257, 2017 Oct.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Initiation and progression of liver fibrosis requires proliferation and activation of resting hepatic stellate cells (HSCs). Cyclin E1 (CcnE1) is the regulatory subunit of the cyclin-dependent kinase 2 (Cdk2) and controls cell cycle re-entry. We have recently shown that genetic inactivation of CcnE1 prevents activation, proliferation, and survival of HSCs and protects from liver fibrogenesis. The aim of the present study was to translate these findings into preclinical applications using an RNA interference (RNAi)-based approach. CcnE1-siRNA (small interfering RNA) efficiently inhibited CcnE1 gene expression in murine and human HSC cell lines and in primary HSCs, resulting in diminished proliferation and increased cell death. In C57BL/6 wild-type (WT) mice, delivery of stabilized siRNA using a liposome-based carrier targeted approximately 95% of HSCs, 70% of hepatocytes, and 40% of CD45 cells after single injection. Acute CCl -mediated liver injury in WT mice induced endogenous CcnE1 expression and proliferation of surviving hepatocytes and nonparenchymal cells, including CD45 leukocytes. Pretreatment with CcnE1-siRNA reverted CcnE1 induction to baseline levels of healthy mice, which was associated with reduced liver injury, diminished proliferation of hepatocytes and leukocytes, and attenuated overall inflammatory response. For induction of liver fibrosis, WT mice were challenged with CCl for 4-6 weeks. Co-treatment with CcnE1-siRNA once a week was sufficient to continuously block CcnE1 expression and cell-cycle activity of hepatocytes and nonparenchymal cells, resulting in significantly ameliorated liver fibrosis and inflammation. Importantly, CcnE1-siRNA also prevented progression of liver fibrosis if applied after onset of chronic liver injury. CONCLUSION: Therapeutic targeting of CcnE1 in vivo using RNAi is feasible and has high antifibrotic activity. (Hepatology 2017;66:1242-1257).
[Mh] Termos MeSH primário: Ciclina E/genética
Terapia Genética
Cirrose Hepática/prevenção & controle
Proteínas Oncogênicas/genética
RNA Interferente Pequeno/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Tetracloreto de Carbono
Proliferação Celular
Ciclina E/antagonistas & inibidores
Células Estreladas do Fígado/efeitos dos fármacos
Hepatócitos/efeitos dos fármacos
Seres Humanos
Hipertrofia
Leucócitos/efeitos dos fármacos
Fígado/patologia
Cirrose Hepática/patologia
Masculino
Camundongos Endogâmicos C57BL
Proteínas Oncogênicas/antagonistas & inibidores
Interferência de RNA
RNA Interferente Pequeno/farmacologia
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin E); 0 (Oncogene Proteins); 0 (RNA, Small Interfering); 0 (cyclin E1, mouse); CL2T97X0V0 (Carbon Tetrachloride)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1002/hep.29275



página 1 de 255 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde