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[PMID]:28653900
[Au] Autor:Wang J; Chen X; Tong S; Zhou H; Sun J; Gou Y; Wu F; Hu J; Xu J; Ding G
[Ad] Endereço:1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, P.R. China.
[Ti] Título:Overexpression of WDFY2 inhibits prostate cancer cell growth and migration via inactivation of Akt pathway.
[So] Source:Tumour Biol;39(6):1010428317704821, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prostate cancer is the most commonly diagnosed malignancy and is the second leading deadly reason among male cancer. WDFY2, which is found to be a cancer-specific fusion gene with CDKN2D in ovarian cancer, is a new gene with unknown function in carcinogenesis. In this study, we investigated the role of WDFY2 in prostate cancer development. We examined WDFY2 expression in human prostate tissue specimens and prostate cancer cell lines BPH-1, LNCaP, PC3, and DU-145. Overexpression of WDFY2 was performed to evaluate the role of WDFY2 in cell proliferation, migration, and colony formation of prostate cancer cells. We analyzed the clinical impact and prognosis of WDFY2 expression on the progress of prostate cancer through data from online datasets. Our results showed that WDFY2 had lower expression level in prostate tumors than in normal tissues. Overexpression of WDFY2 in prostate cancer cells DU145 and PC-3 led to the suppression of cancer cell migration and colony formation. Furthermore, we found that WDFY2 exerted its role by suppressing the activity of Akt pathway other than the epithelial-mesenchymal transition progression. In conclusion, we have uncovered WDFY2 as a tumor suppressor gene and a new potential biomarker for cancer progression. Our results showed that WDFY2 inhibited cancer cell colony formation and migration via suppressing Akt pathway, making it a potential new therapeutic target in prostate cancer.
[Mh] Termos MeSH primário: Proliferação Celular/genética
Transição Epitelial-Mesenquimal/genética
Peptídeos e Proteínas de Sinalização Intracelular/genética
Neoplasias da Próstata/genética
[Mh] Termos MeSH secundário: Idoso
Carcinogênese/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Inibidor de Quinase Dependente de Ciclina p19/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/biossíntese
Masculino
Meia-Idade
Prognóstico
Neoplasias da Próstata/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN2D protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p19); 0 (Intracellular Signaling Peptides and Proteins); 0 (WDFY2 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317704821


  2 / 151 MEDLINE  
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[PMID]:28074012
[Au] Autor:Gamell C; Gulati T; Levav-Cohen Y; Young RJ; Do H; Pilling P; Takano E; Watkins N; Fox SB; Russell P; Ginsberg D; Monahan BJ; Wright G; Dobrovic A; Haupt S; Solomon B; Haupt Y
[Ad] Endereço:Tumour Suppression Laboratory, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000, Australia.
[Ti] Título:Reduced abundance of the E3 ubiquitin ligase E6AP contributes to decreased expression of the INK4/ARF locus in non-small cell lung cancer.
[So] Source:Sci Signal;10(461), 2017 Jan 10.
[Is] ISSN:1937-9145
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor suppressor p16 , one protein encoded by the INK4/ARF locus, is frequently absent in multiple cancers, including non-small cell lung cancer (NSCLC). Whereas increased methylation of the encoding gene (CDKN2A) accounts for its loss in a third of patients, no molecular explanation exists for the remainder. We unraveled an alternative mechanism for the silencing of the INK4/ARF locus involving the E3 ubiquitin ligase and transcriptional cofactor E6AP (also known as UBE3A). We found that the expression of three tumor suppressor genes encoded in the INK4/ARF locus (p15 , p16 , and p19 ) was decreased in E6AP mouse embryo fibroblasts. E6AP induced the expression of the INK4/ARF locus at the transcriptional level by inhibiting CDC6 transcription, a gene encoding a key repressor of the locus. Luciferase assays revealed that E6AP inhibited CDC6 expression by reducing its E2F1-dependent transcription. Chromatin immunoprecipitation analysis indicated that E6AP reduced the amount of E2F1 at the CDC6 promoter. In a subset of NSCLC samples, an E6AP-low/CDC6-high/p16 -low protein abundance profile correlated with low methylation of the gene encoding p16 (CDKN2A) and poor patient prognosis. These findings define a previously unrecognized tumor-suppressive role for E6AP in NSCLC, reveal an alternative silencing mechanism of the INK4/ARF locus, and reveal E6AP as a potential prognostic marker in NSCLC.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/genética
Inibidor de Quinase Dependente de Ciclina p15/genética
Inibidor p16 de Quinase Dependente de Ciclina/genética
Inibidor de Quinase Dependente de Ciclina p19/genética
Neoplasias Pulmonares/genética
Ubiquitina-Proteína Ligases/genética
[Mh] Termos MeSH secundário: Animais
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Carcinoma Pulmonar de Células não Pequenas/patologia
Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Linhagem Celular Tumoral
Células Cultivadas
Inibidor de Quinase Dependente de Ciclina p15/metabolismo
Inibidor p16 de Quinase Dependente de Ciclina/metabolismo
Inibidor de Quinase Dependente de Ciclina p19/metabolismo
Metilação de DNA
Fator de Transcrição E2F1/genética
Fator de Transcrição E2F1/metabolismo
Embrião de Mamíferos/citologia
Fibroblastos/citologia
Fibroblastos/metabolismo
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Estimativa de Kaplan-Meier
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/patologia
Camundongos Knockout
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Regiões Promotoras Genéticas/genética
Ligação Proteica
Ubiquitina-Proteína Ligases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDC6 protein, human); 0 (Cell Cycle Proteins); 0 (Cyclin-Dependent Kinase Inhibitor p15); 0 (Cyclin-Dependent Kinase Inhibitor p16); 0 (Cyclin-Dependent Kinase Inhibitor p19); 0 (E2F1 Transcription Factor); 0 (Nuclear Proteins); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE


  3 / 151 MEDLINE  
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[PMID]:27879259
[Au] Autor:Han X; Zhang J; Peng Y; Peng M; Chen X; Chen H; Song J; Hu X; Ye M; Li J; Sankaran VG; Hillyer CD; Mohandas N; An X; Liu J
[Ad] Endereço:The State Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, Changsha, China.
[Ti] Título:Unexpected role for p19INK4d in posttranscriptional regulation of GATA1 and modulation of human terminal erythropoiesis.
[So] Source:Blood;129(2):226-237, 2017 Jan 12.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Terminal erythroid differentiation is tightly coordinated with cell-cycle exit, which is regulated by cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors (CDKI), yet their roles in erythropoiesis remain to be fully defined. We show here that p19 , a member of CDKI family, is abundantly expressed in erythroblasts and that p19 knockdown delayed erythroid differentiation, inhibited cell growth, and led to increased apoptosis and generation of abnormally nucleated late-stage erythroblasts. Unexpectedly, p19 knockdown did not affect cell cycle. Rather, it led to decreased expression of GATA1 protein. Importantly, the differentiation and nuclear defects were rescued by ectopic expression of GATA1. Because the GATA1 protein is protected by nuclear heat shock protein family (HSP) member HSP70, we examined the effects of p19 knockdown on HSP70 and found that p19 knockdown led to decreased expression of HSP70 and its nuclear localization. The reduced levels of HSP70 are the result of reduced extracellular signal-regulated kinase (ERK) activation. Further biochemical analysis revealed that p19 directly binds to Raf kinase inhibitor PEBP1 and that p19 knockdown increased the expression of PEBP1, which in turn led to reduced ERK activation. Thus we have identified an unexpected role for p19 via a novel PEBP1-p-ERK-HSP70-GATA1 pathway. These findings are likely to have implications for improved understanding of disordered erythropoiesis.
[Mh] Termos MeSH primário: Inibidor de Quinase Dependente de Ciclina p19/metabolismo
Eritropoese/fisiologia
Fator de Transcrição GATA1/metabolismo
Regulação da Expressão Gênica/fisiologia
[Mh] Termos MeSH secundário: Western Blotting
Células Cultivadas
Sangue Fetal
Citometria de Fluxo
Imunofluorescência
Técnicas de Silenciamento de Genes
Seres Humanos
Imunoprecipitação
Reação em Cadeia da Polimerase
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN2D protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p19); 0 (GATA1 Transcription Factor); 0 (GATA1 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-09-739268


  4 / 151 MEDLINE  
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[PMID]:27763644
[Au] Autor:Qu M; Fang F; Zou X; Zeng Q; Fan Z; Chen L; Yue W; Xie X; Pei X
[Ad] Endereço:Stem Cell and Regenerative Medicine Lab, Beijing Institute of Transfusion Medicine, Beijing 100850, China.
[Ti] Título:miR-125b modulates megakaryocyte maturation by targeting the cell-cycle inhibitor p19 .
[So] Source:Cell Death Dis;7(10):e2430, 2016 Oct 20.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A better understanding of the mechanisms involved in megakaryocyte maturation will facilitate the generation of platelets in vitro and their clinical applications. A microRNA, miR-125b, has been suggested to have important roles in the self-renewal of megakaryocyte-erythroid progenitors and in platelet generation. However, miR-125b is also critical for hematopoietic stem cell self-renewal. Thus, the function of miR-125b and the complex signaling pathways regulating megakaryopoiesis remain to be elucidated. In this study, an attentive examination of the endogenous expression of miR-125b during megakaryocyte differentiation was performed. Accordingly, the differentiation of hematopoietic stem cells requires the downregulation of miR-125b, whereas megakaryocyte determination and maturation synchronize with miR-125b accumulation. The overexpression of miR-125b improves megakaryocytic differentiation of K562 and UT-7 cells. Furthermore, stage-specific overexpression of miR-125b in primary cells demonstrates that miR-125b mediates an enhancement of megakaryocytic differentiation after megakaryocyte determination, the stage at which megakaryocytes are negative for the expression of the hematopoietic progenitor marker CD34. The identification of miR-125b targets during megakaryopoiesis was focused on negative regulators of cell cycle because the transition of the G1/S phase has been associated with megakaryocyte polyploidization. Real-time PCR, western blot and luciferase reporter assay reveal that p19 is a direct target of miR-125b. P19 knockdown using small interfering RNA (siRNA) in megakaryocyte-induced K562 cells, UT-7 cells and CD61 promegakaryocytes results in S-phase progression and increased polyploidy, as well as improved megakaryocyte differentiation, similarly to the effects of miR-125b overexpression. P19 overexpression reverses these effects, as indicated by reduced expression of megakaryocyte markers, G1-phase arrest and polyploidy decrease. P19 knockdown in miR-125b downregulated cells or p19 overexpression in miR-125b upregulated cells rescued the effect of miR-125b. Taken together, these findings suggest that miR-125b expression positively regulates megakaryocyte development since the initial phases of megakaryocyte determination, and p19 is one of the key mediators of miR-125b activity during the onset of megakaryocyte polyploidization.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Inibidor de Quinase Dependente de Ciclina p19/genética
Megacariócitos/citologia
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Sequência de Bases
Plaquetas/efeitos dos fármacos
Plaquetas/metabolismo
Ensaio de Unidades Formadoras de Colônias
Inibidor de Quinase Dependente de Ciclina p19/metabolismo
Regulação para Baixo/efeitos dos fármacos
Sangue Fetal/citologia
Fase G1/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Células-Tronco Hematopoéticas/citologia
Células-Tronco Hematopoéticas/efeitos dos fármacos
Células-Tronco Hematopoéticas/metabolismo
Seres Humanos
Células K562
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/efeitos dos fármacos
Leucócitos Mononucleares/metabolismo
Megacariócitos/efeitos dos fármacos
Megacariócitos/metabolismo
MicroRNAs/genética
Poliploidia
Acetato de Tetradecanoilforbol/farmacologia
Regulação para Cima/efeitos dos fármacos
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN2D protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p19); 0 (MIRN125 microRNA, human); 0 (MicroRNAs); NI40JAQ945 (Tetradecanoylphorbol Acetate)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2016.288


  5 / 151 MEDLINE  
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[PMID]:27664376
[Au] Autor:Azzopardi S; Pang S; Klimstra DS; Du YN
[Ad] Endereço:Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY 10065, USA.
[Ti] Título:p53 and p16 /p19 Loss Promotes Different Pancreatic Tumor Types from PyMT-Expressing Progenitor Cells.
[So] Source:Neoplasia;18(10):610-617, 2016 Oct.
[Is] ISSN:1476-5586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In human studies and mouse models, the contributions of p53 and p16 /p19 loss are well established in pancreatic ductal adenocarcinoma (PDAC). Although loss of functional p53 pathway and loss of Ink4a/Arf in human pancreatic acinar cell carcinoma (PACC) and pancreatic neuroendocrine tumor (PanNET) are identified, their direct roles in tumorigenesis of PACC and PanNET remain to be determined. Using transgenic mouse models expressing the viral oncogene polyoma middle T antigen (PyMT), we demonstrate that p53 loss in pancreatic Pdx1+ progenitor cells results in aggressive PACC, whereas Ink4a/Arf loss results in PanNETs. Concurrent loss of p53 and Ink4a/Arf resembles loss of p53 alone, suggesting that Ink4a/Arf loss has no additive effect to PACC progression. Our results show that specific tumor suppressor genotypes provocatively influence the tumor biological phenotypes in pancreatic progenitor cells. Additionally, in a mouse model of ß-cell hyperplasia, we demonstrate that p53 and Ink4a/Arf play cooperative roles in constraining the progression of PanNETs.
[Mh] Termos MeSH primário: Inibidor p16 de Quinase Dependente de Ciclina/deficiência
Inibidor de Quinase Dependente de Ciclina p19/deficiência
Células-Tronco Neoplásicas/metabolismo
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/patologia
Proteína Supressora de Tumor p53/deficiência
[Mh] Termos MeSH secundário: Animais
Transformação Celular Neoplásica/genética
Modelos Animais de Doenças
Feminino
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Estimativa de Kaplan-Meier
Camundongos
Camundongos Transgênicos
Metástase Neoplásica
Tumores Neuroendócrinos/genética
Tumores Neuroendócrinos/mortalidade
Tumores Neuroendócrinos/patologia
Neoplasias Pancreáticas/mortalidade
Fenótipo
Prognóstico
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin-Dependent Kinase Inhibitor p16); 0 (Cyclin-Dependent Kinase Inhibitor p19); 0 (Tumor Suppressor Protein p53)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160925
[St] Status:MEDLINE


  6 / 151 MEDLINE  
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[PMID]:26962681
[Au] Autor:Ma Q; Grati M; Bai F; Pei J; Pei XH; Liu X
[Ad] Endereço:Department of Otolaryngology (D-48), University of Miami Miller School of Medicine, Miami, FL, USA.
[Ti] Título:Rescue from early-onset hearing loss in a mouse model lacking the cyclin-dependent kinase inhibitor p19Ink4d.
[So] Source:Cell Death Dis;7:e2131, 2016 Mar 10.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Inibidor de Quinase Dependente de Ciclina p19/deficiência
Células Ciliadas Auditivas/metabolismo
Perda Auditiva
[Mh] Termos MeSH secundário: Animais
Inibidor de Quinase Dependente de Ciclina p19/metabolismo
Modelos Animais de Doenças
Perda Auditiva/genética
Perda Auditiva/metabolismo
Perda Auditiva/prevenção & controle
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Cdkn2d protein, mouse); 0 (Cyclin-Dependent Kinase Inhibitor p19)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160311
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2016.38


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[PMID]:26854485
[Au] Autor:Largeot A; Perez-Campo FM; Marinopoulou E; Lie-a-Ling M; Kouskoff V; Lacaud G
[Ad] Endereço:Cancer Research UK Stem Cell Biology Group, CR-UK Manchester Institute, University of Manchester, Manchester, UK.
[Ti] Título:Expression of the MOZ-TIF2 oncoprotein in mice represses senescence.
[So] Source:Exp Hematol;44(4):231-7.e4, 2016 Apr.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The MOZ-TIF2 translocation, which fuses monocytic leukemia zinc finger protein (MOZ) histone acetyltransferase (HAT) with the nuclear co-activator TIF2, is associated with the development of acute myeloid leukemia. We recently found that in the absence of MOZ HAT activity, p16(INK4a) transcriptional levels are significantly increased, triggering an early entrance into replicative senescence. Because oncogenic fusion proteins must bypass cellular safeguard mechanisms, such as senescence and apoptosis, to induce leukemia, we hypothesized that this repressive activity of MOZ over p16(INK4a) transcription could be preserved, or even reinforced, in MOZ leukemogenic fusion proteins, such as MOZ-TIF2. We describe here that, indeed, MOZ-TIF2 silences expression of the CDKN2A locus (p16(INK4a) and p19(ARF)), inhibits the triggering of senescence and enhances proliferation, providing conditions favorable to the development of leukemia. Furthermore, we describe that abolishing the MOZ HAT activity of the fusion protein leads to a significant increase in expression of the CDKN2A locus and the number of hematopoietic progenitors undergoing senescence. Finally, we report that inhibition of senescence by MOZ-TIF2 is associated with increased apoptosis, suggesting a role for the fusion protein in p53 apoptosis-versus-senescence balance. Our results underscore the importance of the HAT activity of MOZ, preserved in the fusion protein, for repression of the CDKN2A locus transcription and the subsequent block of senescence, a necessary step for the survival of leukemic cells.
[Mh] Termos MeSH primário: Senescência Celular/genética
Expressão Gênica
Histona Acetiltransferases/genética
Coativador 2 de Receptor Nuclear/genética
Proteínas de Fusão Oncogênicas/genética
[Mh] Termos MeSH secundário: Animais
Inibidor p16 de Quinase Dependente de Ciclina/genética
Inibidor p16 de Quinase Dependente de Ciclina/metabolismo
Inibidor de Quinase Dependente de Ciclina p19/genética
Inibidor de Quinase Dependente de Ciclina p19/metabolismo
Citometria de Fluxo
Loci Gênicos
Histona Acetiltransferases/metabolismo
Camundongos
Coativador 2 de Receptor Nuclear/metabolismo
Proteínas de Fusão Oncogênicas/metabolismo
Proteínas Proto-Oncogênicas c-kit/genética
Proteínas Proto-Oncogênicas c-kit/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Transcrição Genética
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cyclin-Dependent Kinase Inhibitor p16); 0 (Cyclin-Dependent Kinase Inhibitor p19); 0 (Nuclear Receptor Coactivator 2); 0 (Oncogene Proteins, Fusion); 0 (RNA, Messenger); EC 2.3.1.48 (Histone Acetyltransferases); EC 2.3.1.48 (MOZ protein, mouse); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160209
[St] Status:MEDLINE


  8 / 151 MEDLINE  
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[PMID]:26722409
[Au] Autor:Lai R; Li J; Hu P; Wen J; Jie Q; Dong Y; Peng T; Liu X; Xie D
[Ad] Endereço:Department of Otolaryngology Head and Neck Surgery, The Second Xiangya Hospital of Central South University Changsha, China.
[Ti] Título:Role of p19ink4d in the pathogenesis of hearing loss.
[So] Source:Int J Clin Exp Pathol;8(10):12243-51, 2015.
[Is] ISSN:1936-2625
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aimed to investigate the p19 expression in cisplatin-treated rats and the role of p19 in the degeneration of inner ear cells. It also searched for p19 gene alterations in patients with profound sensorineural deafness. P19ink4d is essential for the postmitotic maintenance of hair cells. It is presumed that a mutation in the functional homolog of p19 or a disturbance in its regulated expression can be the underlying cause of hearing loss. Experiments were conducted on male and female Sprague-Dawley rats (aged 6-7 weeks, 280-320 g) with thresholds of auditory brainstem responses <30 dB in the sound pressure level, and signs of middle ear infection were used for the experiment. For clinical evaluation, 400 children (age less than 13 years) from unrelated families with severe or profound sensorineural hearing loss (SNHL) were recruited at the second Xiangya Hospital of Central South University between 2005 and 2013, and genomic DNA for deafness gene analysis was obtained from peripheral blood samples of the patients and their lineal relatives. It was found that the p19 expression increased over time in the inner ear cells after cisplatin administration, but the p19 mRNA and protein levels significantly decreased in rats with manifested hearing loss induced by cisplatin. However, no mutation existed within the coding exons of p19 in the patients with profound sensorineural deafness. To conclude, the results support the concept that p19 may play an important role in the ototoxic effects of cisplatin and is probably involved in the pathogenesis of hearing loss.
[Mh] Termos MeSH primário: Cisplatino/efeitos adversos
Inibidor de Quinase Dependente de Ciclina p19/metabolismo
Perda Auditiva Neurossensorial/patologia
Perda Auditiva/patologia
[Mh] Termos MeSH secundário: Adolescente
Animais
Limiar Auditivo/efeitos dos fármacos
Membrana Basilar/metabolismo
Membrana Basilar/patologia
Criança
Inibidor de Quinase Dependente de Ciclina p19/efeitos dos fármacos
Inibidor de Quinase Dependente de Ciclina p19/genética
Feminino
Células Ciliadas Auditivas Internas/metabolismo
Células Ciliadas Auditivas Internas/patologia
Perda Auditiva/induzido quimicamente
Perda Auditiva/metabolismo
Perda Auditiva Neurossensorial/induzido quimicamente
Perda Auditiva Neurossensorial/metabolismo
Seres Humanos
Masculino
Ratos
Ratos Sprague-Dawley
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CDKN2D protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p19); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160102
[St] Status:MEDLINE


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[PMID]:26240281
[Au] Autor:Nakagawa T; Araki T; Nakagawa M; Hirao A; Unno M; Nakayama K
[Ad] Endereço:Division of Cell Proliferation, ART, Graduate School of Medicine, Tohoku University, Sendai, Japan.
[Ti] Título:S6 Kinase- and ß-TrCP2-Dependent Degradation of p19Arf Is Required for Cell Proliferation.
[So] Source:Mol Cell Biol;35(20):3517-27, 2015 Oct.
[Is] ISSN:1098-5549
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The kinase mTOR (mammalian target of rapamycin) promotes translation as well as cell survival and proliferation under nutrient-rich conditions. Whereas mTOR activates translation through ribosomal protein S6 kinase (S6K) and eukaryotic translation initiation factor 4E-binding protein (4E-BP), how it facilitates cell proliferation has remained unclear. We have now identified p19(Arf), an inhibitor of cell cycle progression, as a novel substrate of S6K that is targeted to promote cell proliferation. Serum stimulation induced activation of the mTOR-S6K axis and consequent phosphorylation of p19(Arf) at Ser(75). Phosphorylated p19(Arf) was then recognized by the F-box protein ß-TrCP2 and degraded by the proteasome. Ablation of ß-TrCP2 thus led to the arrest of cell proliferation as a result of the stabilization and accumulation of p19(Arf). The ß-TrCP2 paralog ß-TrCP1 had no effect on p19(Arf) stability, suggesting that phosphorylated p19(Arf) is a specific substrate of ß-TrCP2. Mice deficient in ß-TrCP2 manifested accumulation of p19(Arf) in the yolk sac and died in utero. Our results suggest that the mTOR pathway promotes cell proliferation via ß-TrCP2-dependent p19(Arf) degradation under nutrient-rich conditions.
[Mh] Termos MeSH primário: Proliferação Celular
Inibidor de Quinase Dependente de Ciclina p19/fisiologia
Células-Tronco Embrionárias Murinas/fisiologia
Proteínas Quinases S6 Ribossômicas 90-kDa/fisiologia
Proteínas Contendo Repetições de beta-Transducina/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Feminino
Células HEK293
Seres Humanos
Masculino
Camundongos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fosforilação
Processamento de Proteína Pós-Traducional
Proteólise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cdkn2d protein, mouse); 0 (Cyclin-Dependent Kinase Inhibitor p19); 0 (Fbxw1b protein, mouse); 0 (beta-Transducin Repeat-Containing Proteins); EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 90-kDa); EC 2.7.11.1 (Rps6ka1 protein, mouse)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150805
[St] Status:MEDLINE
[do] DOI:10.1128/MCB.00343-15


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[PMID]:26019450
[Au] Autor:Zang WQ; Yang X; Wang T; Wang YY; Du YW; Chen XN; Li M; Zhao GQ
[Ad] Endereço:Wen-Qiao Zang, Xuan Yang, Yuan-Yuan Wang, Yu-Wen Du, Xiao-Nan Chen, Min Li, Guo-Qiang Zhao, College of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, Henan Province, China.
[Ti] Título:MiR-451 inhibits proliferation of esophageal carcinoma cell line EC9706 by targeting CDKN2D and MAP3K1.
[So] Source:World J Gastroenterol;21(19):5867-76, 2015 May 21.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: To investigate the underlying molecular mechanisms of miR-451 to inhibit proliferation of esophageal carcinoma cell line EC9706. METHODS: Assays for cell growth, apoptosis and invasion were used to evaluate the effects of miR-451 expression on EC cells. Luciferase reporter and Western blot assays were used to test whether cyclin-dependent kinase inhibitor 2D (CDKN2D) and MAP3K1 act as major targets of miR-451. RESULTS: The results showed that CDKN2D and MAP3K1 are direct targets of miR-451. CDKN2D and MAP3K1 overexpression reversed the effect of miR-451. MiR-451 inhibited the proliferation of EC9706 by targeting CDKN2D and MAP3K1. CONCLUSION: These findings suggest that miR-451 might be a novel prognostic biomarker and a potential target for the treatment of esophageal squamous cell carcinoma in the future.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/enzimologia
Carcinoma/enzimologia
Proliferação Celular
Inibidor de Quinase Dependente de Ciclina p19/metabolismo
Neoplasias Esofágicas/enzimologia
MAP Quinase Quinase Quinase 1/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Carcinoma/genética
Carcinoma/patologia
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/patologia
Linhagem Celular Tumoral
Inibidor de Quinase Dependente de Ciclina p19/genética
Neoplasias Esofágicas/genética
Neoplasias Esofágicas/patologia
Regulação Enzimológica da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
MAP Quinase Quinase Quinase 1/genética
MicroRNAs/genética
Transdução de Sinais
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CDKN2D protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p19); 0 (MIRN451 microRNA, human); 0 (MicroRNAs); EC 2.7.11.25 (MAP Kinase Kinase Kinase 1); EC 2.7.11.25 (MAP3K1 protein, human)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150529
[St] Status:MEDLINE
[do] DOI:10.3748/wjg.v21.i19.5867



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