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[PMID]:28460436
[Au] Autor:Wang W; Jia WD; Hu B; Pan YY
[Ad] Endereço:Department of Medical Oncology, Anhui Provincial Hospital, Anhui Medical University, Hefei 230001, PR China.
[Ti] Título:RAB10 overexpression promotes tumor growth and indicates poor prognosis of hepatocellular carcinoma.
[So] Source:Oncotarget;8(16):26434-26447, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatocellular carcinoma (HCC), one of the most common and lethal cancers worldwide, has a high recurrence rate with current treatment modalities. Identifying biomarkers for early diagnosis and discovering new sufficient molecular targets for the development of targeted therapies are urgently needed. RAB10, a member of the RAS family, has been shown to be highly expressed in HCC. However, the function of RAB10 in HCC is less studied. Here we report that RAB10 acts as an oncogene in HCC. The shRNA-mediated knockdown of RAB10 significantly reduced the proliferation of HCC cells and colony formation, induced cell cycle arrest at G0/G1 phase and increased apoptosis in vitro. In addition, RAB10 knockdown suppressed HCC growth in nude mice. Moreover, RAB10 silencing decreased the phosphorylation of InsR, Met/HGFR, Ron/MST1R, Ret, c-Kit/SCFR, EphA3, EphB4, Tyro3/Dtk, Axl, Tie2/TEK, VEGFR2/KDR, Akt/PKB/Rac, S6 Ribosomal Protein and c-Abl, while the phosphorylation of HSP27, p38 MAPK, Chk2 and TAK1 increased significantly. These results suggest that RAB10 regulates cell survival and proliferation through multiple oncogenic, cell stress and apoptosis pathways. More importantly, high RAB10 expression levels in HCC cells correlated with a poor prognosis in HCC patients. Therefore, our findings revealed an oncogenic role for RAB10 in the pathogenesis of HCC and that RAB10 is a potential molecular target or a biomarker for HCC.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/mortalidade
Expressão Gênica
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/mortalidade
Proteínas rab de Ligação ao GTP/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Pontos de Checagem do Ciclo Celular/genética
Linhagem Celular Tumoral
Proliferação Celular
Sobrevivência Celular
Modelos Animais de Doenças
Feminino
Perfilação da Expressão Gênica
Técnicas de Silenciamento de Genes
Xenoenxertos
Seres Humanos
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Masculino
Camundongos
Gradação de Tumores
Estadiamento de Neoplasias
Oncogenes
Prognóstico
Interferência de RNA
Transdução de Sinais
Estresse Fisiológico
Proteínas rab de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.6.1.- (Rab10 protein, human); EC 3.6.5.2 (rab GTP-Binding Proteins)
[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.15507


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[PMID]:29346433
[Au] Autor:Chen J; OuYang H; An X; Liu S
[Ad] Endereço:Department of E.N.T., West China Hospital, Sichuan University, Chengdu, China.
[Ti] Título:Vault RNAs partially induces drug resistance of human tumor cells MCF-7 by binding to the RNA/DNA-binding protein PSF and inducing oncogene GAGE6.
[So] Source:PLoS One;13(1):e0191325, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Vault is the largest nonicosahedral cytosolic nucleoprotein particle, which is widely involved in induction of chemoresistance and lead to failure in long-term chemotherapy. Vault contains three different major vault proteins (MVPs) and four vault RNAs paralogues (vtRNAs, vtRNA1-1, vtRNA1-2, vtRNA1-3 and vtRNA2-1). Disruption of the MVPs do not induce hypersensitivity while expression of vtRNAs contributes to cells' drug resistance, indicates that vtRNAs, but not MVPs play an important role in causing drug resistance. Polypyrimidine tract binding protein associated splicing factor (PSF) contributes to cell sensitivity to chemotherapy by its transcriptional activity, promotes us to figure out its potential association with vtRNAs. METHODS: We investigate the interaction between PSF and vtRNAs by electrophoretic mobility shift assays (EMSA) and RNA-immunoprecipitation (IP), and showed the binding between PSF and vtRNAs. Chromatin Immunoprecipitation (ChIP) was performed to detect the effects of vtRNAs on the interaction of PSF with GAGE6 promoter. The role of vtRNAs on chemoresistance in MCF-7 was detected by CCK-8 and EdU staining. The independent role of vtRNAs with MVP is detected by MVP or vtRNAs knockdown. RESULTS: The complex with vtRNA1-1 releases PSF, allowing transcription of GAGE6 to proceed. Then we showed that induction of GAGE6 caused drug resistance by promoting cell proliferation and colony formation in soft agar. Ectopic expression of shRNA targets to vtRNA1-1 further confirmed the role of vtRNA1-1 in regulating PSF transcriptional activity independent with the expression of MVP. By vtRNA1-1 or MVP knockdown, it is revealed that vtRNA1-1 caused chemoresistance independent of MVP. Furthermore, knockdown of GAGE6 does not cause drug resistance, indicates the GAGE6 is directly involved in cell proliferation, but not the drug resistance. CONCLUSION: These results suggest that vtRNAs regulates cell proliferation, drug resistance, and possibly other physiological processes of humans, by complex formation with PSF.
[Mh] Termos MeSH primário: Resistência a Medicamentos Antineoplásicos/genética
Oncogenes/genética
Fator de Processamento Associado a PTB/metabolismo
RNA/genética
RNA/metabolismo
Partículas de Ribonucleoproteínas em Forma de Abóbada/genética
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
Doxorrubicina/farmacologia
Seres Humanos
Células MCF-7
Fator de Processamento Associado a PTB/química
Regiões Promotoras Genéticas/genética
Ligação Proteica
Domínios Proteicos
Homologia de Sequência do Ácido Nucleico
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PTB-Associated Splicing Factor); 0 (Vault Ribonucleoprotein Particles); 63231-63-0 (RNA); 80168379AG (Doxorubicin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191325


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[PMID]:29291409
[Au] Autor:Huang J; Deng G; Liu T; Chen W; Zhou Y
[Ad] Endereço:Department of Orthopaedic Surgery, The First Affiliated Hospital of Nanchang University, No. 17 Yong Waizheng Street, Nanchang 330006, China. Electronic address: hj121479@sina.com.
[Ti] Título:Long noncoding RNA PCAT-1 acts as an oncogene in osteosarcoma by reducing p21 levels.
[So] Source:Biochem Biophys Res Commun;495(4):2622-2629, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Long non-coding RNA (lncRNA) is emerging as a critical regulator in multiple cancers. Recently, lncRNA PCAT-1 was found to be up-regulated in prostate cancer and hepatocellular carcinoma, exerting oncogenic effects. However, the biological function and regulatory mechanism of PCAT-1 remain unclear in osteosarcoma (OS). In this study, we reported that PCAT-1 expression was also upregulated in OS tissues, and its overexpression was remarkably associated with tumor size, Enneking stage, tumor node metastasis (TNM) stage and metastasis in patients with OS. Knockdown of PCAT-1 suppressed OS cells proliferation, migration and invasion in vitro, and inhibited the tumorigenicity of OS cells in vivo. Mechanistic investigations revealed that PCAT-1 could interact with EZH2, thereby repressing p21 expression. Additionally, rescue experiments indicated that PCAT-1 functioned as an oncogene partly via suppressing p21 in OS cells. Collectively, our findings demonstrate that PCAT-1 is a new candidate for use in OS diagnosis, prognosis and therapy.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/genética
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Oncogenes/genética
Osteossarcoma/genética
Osteossarcoma/patologia
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Animais
Movimento Celular/genética
Proliferação Celular
Transformação Celular Neoplásica/patologia
Regulação para Baixo/genética
Regulação Neoplásica da Expressão Gênica/genética
Técnicas de Silenciamento de Genes
Terapia Genética/métodos
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Invasividade Neoplásica/genética
Osteossarcoma/terapia
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cdkn1a protein, mouse); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (PCAT-1 lncRNA, human); 0 (RNA, Long Noncoding)
[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:180102
[St] Status:MEDLINE


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[PMID]:28467351
[Au] Autor:Ferraiuolo M; Verduci L; Blandino G; Strano S
[Ad] Endereço:Molecular Chemoprevention and Oncogenomic and Epigenetic Units, Italian National Cancer Institute "Regina Elena", 00144 Rome, Italy. maria.ferraiuolo@ifo.gov.it.
[Ti] Título:Mutant p53 Protein and the Hippo Transducers YAP and TAZ: A Critical Oncogenic Node in Human Cancers.
[So] Source:Int J Mol Sci;18(5), 2017 May 03.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:p53 protein is a well-known tumor suppressor factor that regulates cellular homeostasis. As it has several and key functions exerted, p53 is known as "the guardian of the genome" and either loss of function or gain of function mutations in the coding protein sequence are involved in cancer onset and progression. The Hippo pathway is a key regulator of developmental and regenerative physiological processes but if deregulated can induce cell transformation and cancer progression. The p53 and Hippo pathways exert a plethora of fine-tuned functions that can apparently be in contrast with each other. In this review, we propose that the p53 status can affect the Hippo pathway function by switching its outputs from tumor suppressor to oncogenic activities. In detail, we discuss: (a) the oncogenic role of the protein complex mutant p53/YAP; (b) TAZ oncogenic activation mediated by mutant p53;
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Neoplasias/genética
Fosfoproteínas/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Fatores de Transcrição/metabolismo
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Animais
Carcinogênese/genética
Seres Humanos
Camundongos
Neoplasias/metabolismo
Oncogenes
Fosfoproteínas/genética
Proteínas Serina-Treonina Quinases/genética
Fatores de Transcrição/genética
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Phosphoproteins); 0 (TAZ protein, human); 0 (Transcription Factors); 0 (Tumor Suppressor Protein p53); 0 (YAP1 (Yes-associated) protein, human); EC 2.7.11.1 (Hippo protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29175329
[Au] Autor:Yang X; Qu K; Tao J; Yin G; Han S; Liu Q; Sun H
[Ad] Endereço:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China.
[Ti] Título:Inhibition of CIP2A attenuates tumor progression by inducing cell cycle arrest and promoting cellular senescence in hepatocellular carcinoma.
[So] Source:Biochem Biophys Res Commun;495(2):1807-1814, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CIP2A is a recent identified oncogene that inhibits protein phosphatase 2A (PP2A) and stabilizes c-Myc in cancer cells. To investigate the potential oncogenic role and prognostic value of CIP2A, we comprehensively analyzed the CIP2A expression levels in pan-cancer and observed high expression level of CIP2A in majority cancer types, including hepatocellular carcinoma (HCC). Based on a validation cohort including 60 HCC and 20 non-tumorous tissue samples, we further confirmed the high mRNA and protein expression levels of CIP2A in HCC, and found high CIP2A mRNA expression level was associated with unfavorable overall and recurrence-free survival in patients with HCC. Mechanistic investigations revealed that inhibition of CIP2A significantly attenuated cellular proliferation in vitro and tumourigenicity in vivo. Bioinformatic analysis suggested that CIP2A might be involved in regulating cell cycle. Our experimental data further confirmed CIP2A knockdown induced cell cycle arrest at G1 phase. We found accumulated cellular senescence in HCC cells with CIP2A knockdown, companying expression changes of senescence associated proteins (p21, CDK2, CDK4, cyclin D1, MCM7 and FoxM1). Mechanistically, CIP2A knockdown repressed FoxM1 expression and induced FoxM1 dephosphorylation. Moreover, inhibition of PP2A by phosphatase inhibitor rescued the repression of FoxM1. Taken together, our results showed that CIP2A was highly expressed in HCC. Inhibition of CIP2A induced cell cycle arrest and promoted cellular senescence via repressing FoxM1 transcriptional activity, suggesting a potential anti-cancer target for patients with HCC.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/terapia
Pontos de Checagem do Ciclo Celular/fisiologia
Neoplasias Hepáticas/terapia
Proteínas de Membrana/antagonistas & inibidores
[Mh] Termos MeSH secundário: Autoantígenos/genética
Autoantígenos/fisiologia
Biomarcadores Tumorais/genética
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/patologia
Pontos de Checagem do Ciclo Celular/genética
Linhagem Celular Tumoral
Senescência Celular/genética
Senescência Celular/fisiologia
Progressão da Doença
Proteína Forkhead Box M1/metabolismo
Expressão Gênica
Técnicas de Silenciamento de Genes
Células Hep G2
Seres Humanos
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Proteínas de Membrana/genética
Proteínas de Membrana/fisiologia
Oncogenes
Prognóstico
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Neoplásico/genética
RNA Neoplásico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantigens); 0 (Biomarkers, Tumor); 0 (FOXM1 protein, human); 0 (Forkhead Box Protein M1); 0 (KIAA1524 protein, human); 0 (Membrane Proteins); 0 (RNA, Messenger); 0 (RNA, Neoplasm)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:29313487
[Au] Autor:Eick D
[Ad] Endereço:Department of Molecular Epigenetics, Helmholtz Center Munich, Munich, Germany.
[Ti] Título:Getting to grips with c-Myc.
[So] Source:Elife;7, 2018 01 09.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The transcription factor c-Myc amplifies the transcription of many growth-related genes in cancer cells, but its role as an oncogene is not fully understood.
[Mh] Termos MeSH primário: Oncogenes
Proteínas Proto-Oncogênicas c-myc/genética
[Mh] Termos MeSH secundário: Seres Humanos
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-myc)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE


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[PMID]:28740117
[Au] Autor:Glover TW; Wilson TE; Arlt MF
[Ad] Endereço:Department of Human Genetics; the Department of Pathology; and the Department of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA.
[Ti] Título:Fragile sites in cancer: more than meets the eye.
[So] Source:Nat Rev Cancer;17(8):489-501, 2017 07 25.
[Is] ISSN:1474-1768
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ever since initial suggestions that instability at common fragile sites (CFSs) could be responsible for chromosome rearrangements in cancers, CFSs and associated genes have been the subject of numerous studies, leading to questions and controversies about their role and importance in cancer. It is now clear that CFSs are not frequently involved in translocations or other cancer-associated recurrent gross chromosome rearrangements. However, recent studies have provided new insights into the mechanisms of CFS instability, their effect on genome instability, and their role in generating focal copy number alterations that affect the genomic landscape of many cancers.
[Mh] Termos MeSH primário: Instabilidade Cromossômica
Sítios Frágeis do Cromossomo
Variações do Número de Cópias de DNA
Neoplasias/genética
Oncogenes/genética
[Mh] Termos MeSH secundário: Anáfase
Animais
Quebra Cromossômica
Quebras de DNA de Cadeia Dupla
Replicação do DNA
Rearranjo Gênico
Seres Humanos
Metáfase
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1038/nrc.2017.52


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[PMID]:28982855
[Au] Autor:Bakalova R; Zhelev Z; Shibata S; Nikolova B; Aoki I; Higashi T
[Ad] Endereço:Department of Molecular Imaging and Theranostics, National Institute of Radiological Sciences (NIRS), National Institute for Quantum and Radiological Science and Technology (QST), Chiba, Japan bakalova.rumiana@qst.go.jp.
[Ti] Título:Impressive Suppression of Colon Cancer Growth by Triple Combination SN38/EF24/Melatonin: "Oncogenic" "Onco-Suppressive" Reactive Oxygen Species.
[So] Source:Anticancer Res;37(10):5449-5458, 2017 10.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The study aimed to investigate the effect of multi-targeted combinations (SN38/EF24; SN38/EF24/melatonin) on the growth of colon cancer in experimental animals and their impact on the ratio "oncogenic"/"onco-suppressive" reactive oxygen species (ROS) - a crucial factor for triggering carcinogenesis, as well as for development of effective therapeutic strategies. MATERIALS AND METHODS: The experiments were conducted on colon cancer-grafted mice - non-treated, SN38/EF24-treated and SN38/EF24/melatonin-treated within 22 days. The balance between different types of ROS was measured in vivo by nitroxide-enhanced magnetic resonance imaging (MRI), as well as on isolated tissue specimens by conventional analytical tests. RESULTS: Both combinations significantly suppressed the tumor growth. Impressive anticancer effect was observed in SN38/EF24/melatonin-treated mice - almost complete destruction of the tumor. Both types of ROS (superoxide and hydroperoxides) were elevated in cancer, but the MRI data suggest that the ratio between them tends towards superoxide. SN38/EF24 decreased the level of superoxide, but did not affect the level of hydroperoxides in the cancerous tissue, while SN38/EF24/melatonin decreased the level of superoxide below the control and increased significantly the level of hydroperoxides. CONCLUSION: The most important observations are that: (i) colon cancer was characterized by a vicious cycle, that ensures a permanent domination of "oncogenic" ROS (as superoxide) over "onco-suppressive" ROS (as hydrogen peroxide); (ii) the anticancer effect of the triple combination EF24/SN38/melatonin was accompanied by decreasing "oncogenic" and increasing "onco-suppressive" ROS; (iii) the ratio between both types of ROS could be a new onco-target for combined therapy; and (iv) nitroxide-enhanced MRI is a valuable tool for analyzing of this ratio.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Compostos de Benzilideno/farmacologia
Camptotecina/análogos & derivados
Proliferação Celular/efeitos dos fármacos
Neoplasias Colorretais/tratamento farmacológico
Melatonina/farmacologia
Oncogenes
Estresse Oxidativo/efeitos dos fármacos
Piperidonas/farmacologia
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Camptotecina/farmacologia
Linhagem Celular Tumoral
Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Peróxido de Hidrogênio/metabolismo
Imagem por Ressonância Magnética
Masculino
Camundongos Endogâmicos BALB C
Camundongos Nus
Transdução de Sinais/efeitos dos fármacos
Superóxidos/metabolismo
Fatores de Tempo
Carga Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3,5-bis(2-fluorobenzylidene)piperidin-4-one); 0 (Benzylidene Compounds); 0 (Piperidones); 0 (Reactive Oxygen Species); 11062-77-4 (Superoxides); 7673326042 (irinotecan); BBX060AN9V (Hydrogen Peroxide); JL5DK93RCL (Melatonin); XT3Z54Z28A (Camptothecin)
[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:171007
[St] Status:MEDLINE


  9 / 14393 MEDLINE  
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[PMID]:28982852
[Au] Autor:Lim HS; Kim CS; Kim JS; Yu SK; Go DS; Lee SA; Moon SM; Chun HS; Kim SG; Kim DK
[Ad] Endereço:Oral Biology Research Institute, School of Dentistry, Chosun University, Gwangju, Republic of Korea.
[Ti] Título:Suppression of Oral Carcinoma Oncogenic Activity by microRNA-203 Down-regulation of .
[So] Source:Anticancer Res;37(10):5425-5433, 2017 10.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The purpose of this study was to elucidate the molecular mechanism underlying regulation of semaphorin-6A (SEMA6A) involving microRNA-203 (miR-203) as a tumor suppressor in YD-38 human oral cancer cells. MATERIALS AND METHODS: miRNA arrays, polymerase chain reaction analyses, MTT assays, immunoblotting, and luciferase assays were carried out in YD-38 cells. RESULTS: MiRNA microarray results showed that expression of miR-203 was significantly down-regulated in YD-38 cells compared to normal human oral keratinocytes. The viability of YD-38 cells was reduced by miR-203 in time- and dose-dependent manners. Overexpression of miR-203 increased the nuclear condensation of YD-38 cells and activated the apoptotic signaling pathway by up-regulating pro-apoptotic factors, such as BCL-2-associated X protein (BAX) and BCL-2 homologous antagonist killer (BAK), and the active forms of caspase-9, caspase-3, and poly-(ADP-ribose)-polymerase (PARP). Furthermore, target gene array analyses revealed that the expression of class 6 semaphorin A (SEMA6A) was down-regulated by miR-203 in YD-38 cells. Both the mRNA and protein levels of SEMA6A were reduced in YD-38 cells transfected with miR-203. Luciferase activity assay confirmed that miR-203 directly targets the SEMA6A 3'-untranslated region to suppress gene expression. CONCLUSION: Our results indicate that miR-203 induces the apoptosis of YD-38 human oral cancer cells by directly targeting SEMA6A, suggesting its potential application in anticancer therapeutics.
[Mh] Termos MeSH primário: MicroRNAs/metabolismo
Neoplasias Bucais/metabolismo
Oncogenes
Semaforinas/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Apoptose
Proteínas Reguladoras de Apoptose/metabolismo
Sítios de Ligação
Linhagem Celular Tumoral
Proliferação Celular
Sobrevivência Celular
Regulação para Baixo
Regulação Enzimológica da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
MicroRNAs/genética
Neoplasias Bucais/genética
Neoplasias Bucais/patologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Semaforinas/genética
Transdução de Sinais
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Apoptosis Regulatory Proteins); 0 (MIRN203 microRNA, human); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (SEMA6A protein, human); 0 (Semaphorins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE


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[PMID]:28981588
[Au] Autor:Phesse TJ; Durban VM; Sansom OJ
[Ad] Endereço:European Cancer Stem Cell Research Institute, Cardiff University, Cardiff, South Glamorgan, CF24 4HQ, UK.
[Ti] Título:Defining key concepts of intestinal and epithelial cancer biology through the use of mouse models.
[So] Source:Carcinogenesis;38(10):953-965, 2017 Oct 01.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Over the past 20 years, huge advances have been made in modelling human diseases such as cancer using genetically modified mice. Accurate in vivo models are essential to examine the complex interaction between cancer cells, surrounding stromal cells, tumour-associated inflammatory cells, fibroblast and blood vessels, and to recapitulate all the steps involved in metastasis. Elucidating these interactions in vitro has inherent limitations, and thus animal models are a powerful tool to enable researchers to gain insight into the complex interactions between signalling pathways and different cells types. This review will focus on how advances in in vivo models have shed light on many aspects of cancer biology including the identification of oncogenes, tumour suppressors and stem cells, epigenetics, cell death and context dependent cell signalling.
[Mh] Termos MeSH primário: Epitélio/patologia
Neoplasias Intestinais/metabolismo
Neoplasias Intestinais/patologia
Neoplasias Experimentais/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Sistemas CRISPR-Cas
Modelos Animais de Doenças
Genes Supressores de Tumor
Seres Humanos
Neoplasias Intestinais/genética
Metilação
Camundongos
Camundongos Transgênicos
Neoplasias Experimentais/genética
Neoplasias Experimentais/metabolismo
Células-Tronco Neoplásicas/patologia
Oncogenes
Transdução de Sinais
Células-Tronco/metabolismo
Células-Tronco/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgx080



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