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  1 / 14943 MEDLINE  
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[PMID]:29421442
[Au] Autor:Wu S; Mao L; Li Y; Yin Y; Yuan W; Chen Y; Ren W; Lu X; Li Y; Chen L; Chen B; Xu W; Tian T; Lu Y; Jiang L; Zhuang X; Chu M; Wu J
[Ad] Endereço:Jiangsu Provincial Key Laboratory of Geriatrics, Department of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
[Ti] Título:RAGE may act as a tumour suppressor to regulate lung cancer development.
[So] Source:Gene;651:86-93, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Although the correlation of the RAGE rs2070600 polymorphism and cancer risk has been confirmed, detailed studies with functional and experimental evaluations are lacking. In this study, we first aimed to examine whether this polymorphism is associated with cancer risk based on the latest published data, and consistent with previous meta-analyses, a significant association between the rs2070600 polymorphism and cancer risk was observed (A versus G: OR = 1.25; 95% CI = 1.12-1.40). In additional stratified analyses based on cancer type, rs2070600 was significantly associated with an increased risk of lung cancer (A versus G: OR = 1.20; 95% CI = 1.09-1.33). Moreover, TCGA database showed that the expression level of RAGE was significantly lower in lung cancer tumour tissues than in adjacent non-tumour tissues, which was validated in the GEO database. Additionally, eQTL analysis indicated that the rs2070600 polymorphism may modify the expression level of RAGE in lung squamous cell carcinoma tissues (P = 0.09). Finally, we performed functional experiments in lung cancer cells and preliminarily demonstrated that RAGE may act as a tumour suppressor in lung cancer development. These findings provide evidence that the variant A allele of rs2070600 may decrease the expression of the tumour suppressor gene RAGE, thereby increasing lung cancer risk.
[Mh] Termos MeSH primário: Genes Supressores de Tumor
Neoplasias Pulmonares/genética
Polimorfismo de Nucleotídeo Único
Receptor para Produtos Finais de Glicação Avançada/genética
[Mh] Termos MeSH secundário: Linhagem Celular
Linhagem Celular Tumoral
Expressão Gênica
Predisposição Genética para Doença
Seres Humanos
Neoplasias Pulmonares/patologia
Fenótipo
Locos de Características Quantitativas
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Receptor for Advanced Glycation End Products)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE


  2 / 14943 MEDLINE  
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[PMID]:29408272
[Au] Autor:Saif I; Kasmi Y; Allali K; Ennaji MM
[Ad] Endereço:Team of Virology, Oncology and Medical Biotechnologies, Laboratory of Virology, Microbiology, Quality and Biotechnologies/ETB, Faculty of Science sand Technologies-Mohammedia, Hassan II University of Casablanca, Morocco.
[Ti] Título:Prediction of DNA methylation in the promoter of gene suppressor tumor.
[So] Source:Gene;651:166-173, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The epigenetics methylation of cytosine is the most common epigenetic form in DNA sequences. It is highly concentrated in the promoter regions of the genes, leading to an inactivation of tumor suppressors regardless of their initial function. In this work, we aim to identify the highly methylated regions; the cytosine-phosphate-guanine (CpG) island located on the promoters and/or the first exon gene known for their key roles in the cell cycle, hence the need to study gene-gene interactions. The Frommer and hidden Markov model algorithms are used as computational methods to identify CpG islands with specificity and sensitivity up to 76% and 80%, respectively. The results obtained show, on the one hand, that the genes studied are suspected of developing hypermethylation in the promoter region of the gene involved in the case of a cancer. We then showed that the relative richness in CG results from a high level of methylation. On the other hand, we observe that the gene-gene interaction exhibits co-expression between the chosen genes. This let us to conclude that the hidden Markov model algorithm predicts more specific and valuable information about the hypermethylation in gene as a preventive and diagnostics tools for the personalized medicine; as that the tumor-suppresser-genes have relative co-expression and complementary relations which the hypermethylation affect in the samples studied in our work.
[Mh] Termos MeSH primário: Biologia Computacional/métodos
Ilhas de CpG
Metilação de DNA
Genes Supressores de Tumor
Regiões Promotoras Genéticas
[Mh] Termos MeSH secundário: Algoritmos
DNA de Neoplasias
Conjuntos de Dados como Assunto
Epistasia Genética
Seres Humanos
Cadeias de Markov
Modelos Genéticos
Neoplasias/genética
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Neoplasm)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  3 / 14943 MEDLINE  
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[PMID]:27773925
[Au] Autor:Visconte V; Przychodzen B; Han Y; Nawrocki ST; Thota S; Kelly KR; Patel BJ; Hirsch C; Advani AS; Carraway HE; Sekeres MA; Maciejewski JP; Carew JS
[Ad] Endereço:Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.
[Ti] Título:Complete mutational spectrum of the autophagy interactome: a novel class of tumor suppressor genes in myeloid neoplasms.
[So] Source:Leukemia;31(2):505-510, 2017 02.
[Is] ISSN:1476-5551
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Autofagia/genética
Neoplasias da Medula Óssea/genética
Mutação
[Mh] Termos MeSH secundário: Genes Supressores de Tumor
Seres Humanos
Transtornos Mieloproliferativos/genética
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180310
[Lr] Data última revisão:
180310
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/leu.2016.295


  4 / 14943 MEDLINE  
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[PMID]:29288362
[Au] Autor:Goonesekere NCW; Andersen W; Smith A; Wang X
[Ad] Endereço:Department of Chemistry and Biochemistry, University of Northern Iowa, 1227 W. 27th Street, Cedar Falls, IA, 50613-0423, USA. nalin.goonesekere@uni.edu.
[Ti] Título:Identification of genes highly downregulated in pancreatic cancer through a meta-analysis of microarray datasets: implications for discovery of novel tumor-suppressor genes and therapeutic targets.
[So] Source:J Cancer Res Clin Oncol;144(2):309-320, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The lack of specific symptoms at early tumor stages, together with a high biological aggressiveness of the tumor contribute to the high mortality rate for pancreatic cancer (PC), which has a 5-year survival rate of about 7%. Recent failures of targeted therapies inhibiting kinase activity in clinical trials have highlighted the need for new approaches towards combating this deadly disease. METHODS: In this study, we have identified genes that are significantly downregulated in PC, through a meta-analysis of large number of microarray datasets. We have used qRT-PCR to confirm the downregulation of selected genes in a panel of PC cell lines. RESULTS: This study has yielded several novel candidate tumor-suppressor genes (TSGs) including GNMT, CEL, PLA2G1B and SERPINI2. We highlight the role of GNMT, a methyl transferase associated with the methylation potential of the cell, and CEL, a lipase, as potential therapeutic targets. We have uncovered genetic links to risk factors associated with PC such as smoking and obesity. Genes important for patient survival and prognosis are also discussed, and we confirm the dysregulation of metabolic pathways previously observed in PC. CONCLUSIONS: While many of the genes downregulated in our dataset are associated with protein products normally produced by the pancreas for excretion, we have uncovered some genes whose downregulation appear to play a more causal role in PC. These genes will assist in providing a better understanding of the disease etiology of PC, and in the search for new therapeutic targets and biomarkers.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Genes Supressores de Tumor
Neoplasias Pancreáticas/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Conjuntos de Dados como Assunto
Regulação para Baixo
Seres Humanos
Terapia de Alvo Molecular
Análise de Sequência com Séries de Oligonucleotídeos
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[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:171231
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2558-4


  5 / 14943 MEDLINE  
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[PMID]:28460460
[Au] Autor:Valdés-Mora F; Locke WJ; Bandrés E; Gallego-Ortega D; Cejas P; García-Cabezas MA; Colino-Sanguino Y; Feliú J; Del Pulgar TG; Lacal JC
[Ad] Endereço:Histone Variants Group, Epigenetics Research Program, Genomics and Epigenetics Division, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
[Ti] Título:Clinical relevance of the transcriptional signature regulated by CDC42 in colorectal cancer.
[So] Source:Oncotarget;8(16):26755-26770, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CDC42 is an oncogenic Rho GTPase overexpressed in colorectal cancer (CRC). Although CDC42 has been shown to regulate gene transcription, the specific molecular mechanisms regulating the oncogenic ability of CDC42 remain unknown. Here, we have characterized the transcriptional networks governed by CDC42 in the CRC SW620 cell line using gene expression analysis. Our results establish that several cancer-related signaling pathways, including cell migration and cell proliferation, are regulated by CDC42. This transcriptional signature was validated in two large cohorts of CRC patients and its clinical relevance was also studied. We demonstrate that three CDC42-regulated genes offered a better prognostic value when combined with CDC42 compared to CDC42 alone. In particular, the concordant overexpression of CDC42 and silencing of the putative tumor suppressor gene CACNA2D2 dramatically improved the prognostic value. The CACNA2D2/CDC42 prognostic classifier was further validated in a third CRC cohort as well as in vitro and in vivo CRC models. Altogether, we show that CDC42 has an active oncogenic role in CRC via the transcriptional regulation of multiple cancer-related pathways and that CDC42-mediated silencing of CACNA2D2 is clinically relevant. Our results further support the use of CDC42 specific inhibitors for the treatment of the most aggressive types of CRC.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Regulação Neoplásica da Expressão Gênica
Transcriptoma
Proteína cdc42 de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Canais de Cálcio/genética
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Neoplasias Colorretais/diagnóstico
Neoplasias Colorretais/mortalidade
Modelos Animais de Doenças
Feminino
Perfilação da Expressão Gênica
Redes Reguladoras de Genes
Genes Supressores de Tumor
Xenoenxertos
Seres Humanos
Camundongos
Gradação de Tumores
Metástase Neoplásica
Estadiamento de Neoplasias
Prognóstico
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CACNA2D2 protein, human); 0 (Calcium Channels); EC 3.6.5.2 (cdc42 GTP-Binding Protein)
[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.15815


  6 / 14943 MEDLINE  
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[PMID]:28460450
[Au] Autor:Yi JM; Kang EJ; Kwon HM; Bae JH; Kang K; Ahuja N; Yang K
[Ad] Endereço:Research Center, Dongnam Institute of Radiological and Medical Sciences (DIRAMS), Busan, Republic of Korea.
[Ti] Título:Epigenetically altered miR-1247 functions as a tumor suppressor in pancreatic cancer.
[So] Source:Oncotarget;8(16):26600-26612, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Altered expression of microRNAs has been strongly implicated in human cancers, and growing evidence is emerging that a number of miRNAs are downregulated in cancer associated with CpG island hypermethylation. Although pancreatic cancer is one of the most malignant human cancers, the roles of miRNAs underlying the tumorigenesis of pancreatic cancer are still poorly understood. In the present study, we explored the molecular functional role of microRNA-1247 as tumor suppressor associated with epigenetic alteration in pancreatic cancer. CpG islands methylation of miR-1247 is frequently observed in various pancreatic cancer cell lines and in primary pancreatic tumors, but not in normal pancreatic tissue. Ectopic expression of miR-1247 in five pancreatic cancer cell lines results in suppressing of cell growth, proliferation, migration, and invasion in vitro and tumorigenicity of pancreatic cancer cells in vivo. Interestingly, we found one putative target gene of miR-1247, regulator of chromosome condensation 2 (RCC2), harbored miR-1247 target sequences in the 3' UTR of its mRNA. In functional studies in vitro to understand the interaction between miR-1247 and RCC2, decreasing of RCC2 gene expression by miR-1247 was observed by immunoblotting and immunohistochemistry at both mRNA and protein levels. Moreover, luciferase reporter assay confirmed that RCC2 was a direct target of miR-1247. Taken together, our data suggest that CpG island hypermethylation of miR-1247 is responsible for its downregulation in pancreatic cancer, and ectopic expression of miR-1247 functions as a potential tumor suppressor targeting RCC2 in pancreatic cancer cells.
[Mh] Termos MeSH primário: Epigênese Genética
Regulação Neoplásica da Expressão Gênica
Genes Supressores de Tumor
MicroRNAs/genética
Neoplasias Pancreáticas/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular
Proteínas Cromossômicas não Histona/genética
Ilhas de CpG
Metilação de DNA
Inativação Gênica
Fatores de Troca do Nucleotídeo Guanina/genética
Seres Humanos
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromosomal Proteins, Non-Histone); 0 (Guanine Nucleotide Exchange Factors); 0 (MIRN1247 microRNA, human); 0 (MicroRNAs); 0 (RCC2 protein, human)
[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.15722


  7 / 14943 MEDLINE  
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[PMID]:29278705
[Au] Autor:Yamamoto JI; Kasamatsu A; Okubo Y; Nakashima D; Fushimi K; Minakawa Y; Kasama H; Shiiba M; Tanzawa H; Uzawa K
[Ad] Endereço:Department of Oral Science, Graduate School of Medicine, Chiba University, Chiba, Japan.
[Ti] Título:Evaluation of tryptophan-aspartic acid repeat-containing protein 34 as a novel tumor-suppressor molecule in human oral cancer.
[So] Source:Biochem Biophys Res Commun;495(4):2469-2474, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tryptophan-aspartic acid (WD) repeat-containing protein 34 (WDR34), one of the WDR protein superfamilies with five WD40 domains, inhibits a transforming growth factor-beta (TGF-ß) activated kinase 1 (TAK1)-associated NF-κB activation pathway. Nevertheless, little is known about the roles of WDR34 in cancer. The current study sought to elucidate the clinical relevance of WDRsfb34 in oral squamous cell carcinoma (OSCC). We found WDR34 down-regulation in OSCCs compared with normal control tissues using real-time quantitative reverse transcription-polymerase chain reaction, immunoblotting, and immunohistochemistry. Models of overexpression of WDR34 (oeWDR34) showed depressed cellular growth through cell-cycle arrest at the G1 phase. To investigate the inhibitory function of WDR34, we challenged oeWDR34 cells with interleukin (IL)-1, a ligand for activation of the TAK1-NF-κB pathway and assessed the expression of a target gene of the pathway. oeWDR34 strongly inhibited IL-6 expression, which is closely related to tumoral growth, compared with control cells, suggesting that WDR34 would be a critical molecule for control of tumoral progression. In addition to the in vitro experiments, WDR34 negativity was correlated with tumoral growth of OSCCs. Our findings suggested that WDR34 inhibits OSCC progression and might be a potential tumor-suppressor molecule in OSCCs.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/patologia
Proteínas de Transporte/metabolismo
Neoplasias Bucais/metabolismo
Neoplasias Bucais/patologia
[Mh] Termos MeSH secundário: Apoptose/genética
Carcinoma de Células Escamosas/genética
Proteínas de Transporte/genética
Genes Supressores de Tumor
Seres Humanos
Neoplasias Bucais/genética
Resultado do Tratamento
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (WDR34 protein, human)
[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:171227
[St] Status:MEDLINE


  8 / 14943 MEDLINE  
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[PMID]:29374692
[Au] Autor:Jung YY; Sung JY; Kim JY; Kim HS
[Ad] Endereço:Department of Pathology, Myongji Hospital, Goyang, Republic of Korea.
[Ti] Título:Down-regulation of B-Cell Translocation Gene 1 by Promoter Methylation in Colorectal Carcinoma.
[So] Source:Anticancer Res;38(2):691-697, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: B-cell translocation gene 1 (BTG1) acts as a tumour suppressor in human malignancies. However, the precise mechanism of BTG1 down-regulation in colorectal carcinoma (CRC) remains unclear. We analyzed BTG1 expression in CRC cell lines and tissues and investigated the mechanism underlying the observed alterations. MATERIALS AND METHODS: Real-time polymerase chain reaction (PCR) and western blot analyses were performed to analyze BTG1 expression in CRC cell lines. The methylation status of the BTG1 promoter region in cell lines was determined by methylation-specific PCR, and the effect of demethylation on BTG1 expression was explored with 5-aza-deoxycytidine treatment. BTG1 protein expression in CRC tissue samples was evaluated using immunostaining. RESULTS: CRC cell lines and tissue samples expressed lower levels of BTG1 compared to controls, and BTG1 levels were significantly lower in metastatic than primary CRC. In BTG1-down-regulated CRC cell lines, the BTG1 promoter was highly methylated, and 5-aza-deoxycytidine significantly restored BTG1 expression. CONCLUSION: BTG1 down-regulation in CRC occurs through epigenetic repression, which is involved in the development and progression of CRC.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Metilação de DNA
Proteínas de Neoplasias/genética
Regiões Promotoras Genéticas
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/genética
Estudos de Casos e Controles
Linhagem Celular Tumoral
Neoplasias Colorretais/patologia
Regulação para Baixo/genética
Regulação Neoplásica da Expressão Gênica
Genes Supressores de Tumor
Seres Humanos
Proteínas de Neoplasias/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Neoplasm Proteins); 146835-72-5 (BTG1 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  9 / 14943 MEDLINE  
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[PMID]:28470677
[Au] Autor:Tang H; Wei P; Chang P; Li Y; Yan D; Liu C; Hassan M; Li D
[Ad] Endereço:Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX.
[Ti] Título:Genetic polymorphisms associated with pancreatic cancer survival: a genome-wide association study.
[So] Source:Int J Cancer;141(4):678-686, 2017 08 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous findings on the association of genetic factors and pancreatic cancer survival are limited and inconsistent. In a two-stage study, we analyzed the existing genome-wide association study dataset of 868 pancreatic cancer patients from MD Anderson Cancer Center in relation to overall survival using Cox regression. Top hits were selected for replication in another 820 patients from the same institution using the Taqman genotyping method. Functional annotation, pathway analysis and gene expression analysis were conducted using existing software and databases. We discovered genome-wide significant associations of patient survival with three imputed SNPs which, in complete LD (r = 1), were intronic SNPs of the PAIP2B (rs113988120) and DYSF genes (rs112493246 and rs138529893) located on Chromosome 2. The variant alleles were associated with a 3.06-fold higher risk of death [95% confidence interval (CI) = 2.10-4.47, p=6.4 × 10-9] after adjusting for clinical factors. Eleven SNPs were tested in the replication study and the association of rs113988120 with survival was confirmed (hazard ratio: 1.57, 95% CI: 1.13-2.20,  p=0.008). In silico analysis found rs1139988120 might lead to altered motif. This locus is in LD (D' = 0.77) with three eQTL SNPs near or belong to the NAGK and MCEE genes. According to The Cancer Genome Atlas data and our previous RNA-sequencing data, the mRNA expression level of PAIP2B but not NAGK, MCEE or DYSF was significantly lower in pancreatic tumors than in normal adjacent tissues. Additional validation efforts and functional studies are warranted to demonstrate whether PAIP2B is a novel tumor suppressor gene and a potential therapeutic target for pancreatic cancer.
[Mh] Termos MeSH primário: Regulação para Baixo
Neoplasias Pancreáticas/genética
Polimorfismo de Nucleotídeo Único
Proteínas Repressoras/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Cromossomos Humanos Par 2/genética
Disferlina
Feminino
Regulação Neoplásica da Expressão Gênica
Genes Supressores de Tumor
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Masculino
Proteínas de Membrana/genética
Meia-Idade
Proteínas Musculares/genética
Análise de Regressão
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DYSF protein, human); 0 (Dysferlin); 0 (Membrane Proteins); 0 (Muscle Proteins); 0 (Repressor Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30762


  10 / 14943 MEDLINE  
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[PMID]:28746790
[Au] Autor:Zhang J; Li Z; Liu L; Wang Q; Li S; Chen D; Hu Z; Yu T; Ding J; Li J; Yao M; Huang S; Zhao Y; He X
[Ad] Endereço:Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
[Ti] Título:Long noncoding RNA TSLNC8 is a tumor suppressor that inactivates the interleukin-6/STAT3 signaling pathway.
[So] Source:Hepatology;67(1):171-187, 2018 01.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Long noncoding RNAs can serve as oncogenes or tumor suppressors in human cancer; however, their biological functions and underlying mechanism in hepatocarcinogenesis are largely unknown. Here, we report a novel tumor suppressor long noncoding RNA on chromosome 8p12 (termed TSLNC8) that is frequently deleted and down-regulated in hepatocellular carcinoma (HCC) tissues. The loss of TSLNC8 is highly associated with the malignant features of HCC and serves as a prognostic indicator for HCC patients. TSLNC8 significantly suppresses the proliferation and metastasis of HCC cells in vitro and in vivo. TSLNC8 exerts its tumor suppressive activity by competitively interacting with transketolase and signal transducer and activator of transcription 3 (STAT3) and modulating the STAT3-Tyr705 and STAT3-Ser727 phosphorylation levels and STAT3 transcriptional activity, thus resulting in inactivation of the interleukin-6-STAT3 signaling pathway in HCC cells. CONCLUSION: TSLNC8 is a promising prognostic predictor for patients with HCC, and the TSLNC8-transketolase-STAT3 axis is a potential therapeutic target for HCC treatment. (Hepatology 2018;67:171-187).
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Carcinoma Hepatocelular/patologia
Interleucina-6/metabolismo
Neoplasias Hepáticas/patologia
RNA Longo não Codificante/metabolismo
Fator de Transcrição STAT3/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Biópsia por Agulha
Carcinoma Hepatocelular/metabolismo
Linhagem Celular Tumoral
Receptor gp130 de Citocina/metabolismo
Regulação para Baixo
Genes Supressores de Tumor
Seres Humanos
Imuno-Histoquímica
Neoplasias Hepáticas/metabolismo
Fosforilação
Projetos Piloto
Prognóstico
Modelos de Riscos Proporcionais
RNA Longo não Codificante/genética
Curva ROC
Fator de Transcrição STAT3/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (IL6ST protein, human); 0 (Interleukin-6); 0 (RNA, Long Noncoding); 0 (STAT3 Transcription Factor); 133483-10-0 (Cytokine Receptor gp130)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1002/hep.29405



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