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[PMID]:29385191
[Au] Autor:Chuerduangphui J; Ekalaksananan T; Chaiyarit P; Patarapadungkit N; Chotiyano A; Kongyingyoes B; Promthet S; Pientong C
[Ad] Endereço:Department of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
[Ti] Título:Effects of arecoline on proliferation of oral squamous cell carcinoma cells by dysregulating c-Myc and miR-22, directly targeting oncostatin M.
[So] Source:PLoS One;13(1):e0192009, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arecoline, the major alkaloid of areca nut, is known to induce oral carcinogenesis, however, its mechanism is still needed to elucidate. This study investigated the effects of arecoline on cell viability and cell-cycle progression of oral squamous cell carcinoma (OSCC) cells as well as a relevant cellular gene expression. The results showed that a low concentration of arecoline (0.025 µg/ml) increased OSCC cell viability, proportion of cells in G2/M phase and cell proliferation. Simultaneously, it induced IL-6, STAT3 and c-Myc expression. Interestingly, c-myc promoter activity was also induced by arecoline. MiR-22 expression in arecoline-treated OSCC cells was suppressed and comparable to an upregulated c-Myc expression. In arecoline-treated OSCC cells, oncostatin M (OSM) expression was significantly upregulated and inversely correlated with miR-22 expression. Likewise, OSM expression and its post-transcriptional activity were significantly decreased in miR-22-transfected OSCC and 293FT cells. This result demonstrated that miR-22 directly targeted OSM. Interestingly, miR-22 played an important role as a tumor suppresser on suppressing cell proliferation, migration and cell-cycle progression of OSCC cells. This result suggested the effect of arecoline to promote cell proliferation and cell-cycle progression of OSCC cells might be involved in induction of c-Myc expression and reduction of miR-22 resulting in OSM upregulation.
[Mh] Termos MeSH primário: Arecolina/farmacologia
Carcinoma de Células Escamosas/patologia
Proliferação Celular/efeitos dos fármacos
MicroRNAs/metabolismo
Neoplasias Bucais/patologia
Proteínas Proto-Oncogênicas c-myc/metabolismo
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/metabolismo
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Seres Humanos
Interleucina-6/biossíntese
MicroRNAs/genética
Neoplasias Bucais/metabolismo
Regiões Promotoras Genéticas
Proteínas Proto-Oncogênicas c-myc/genética
Fator de Transcrição STAT3/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-6); 0 (MIRN22 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-myc); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 4ALN5933BH (Arecoline)
[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:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192009


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[PMID]:29339161
[Au] Autor:El Nagar S; Zindy F; Moens C; Martin L; Plassard D; Roussel MF; Lamonerie T; Billon N
[Ad] Endereço:Université Côte d'Azur, CNRS, Inserm, iBV, Nice, France.
[Ti] Título:A new genetically engineered mouse model of choroid plexus carcinoma.
[So] Source:Biochem Biophys Res Commun;496(2):568-574, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Choroid plexus carcinomas (CPCs) are highly malignant brain tumours predominantly found in children and associated to poor prognosis. Improved therapy for these cancers would benefit from the generation of animal models. Here we have created a novel mouse CPC model by expressing a stabilised form of c-Myc (MycT58A) and inactivating Trp53 in the choroid plexus of newborn mice. This induced aberrant proliferation of choroid plexus epithelial cells, leading to aggressive tumour development and death within 150 days. Choroid plexus tumours occurred with a complete penetrance in all brain ventricles, with prevalence in the lateral and fourth ventricles. Histological and cellular analysis indicated that these tumours were CPCs resembling their human counterparts. Comparison of gene expression profiles of CPCs and non-neoplastic tissues revealed profound alterations in cell cycle regulation and DNA damage responses, suggesting that dysregulation of cell division and DNA checkpoint pathways may represent key vulnerabilities. This novel animal model of CPC provides an invaluable tool to elucidate the mechanism of CPC formation and to develop successful therapies against this devastating paediatric cancer.
[Mh] Termos MeSH primário: Carcinoma/genética
Carcinoma/patologia
Neoplasias do Plexo Corióideo/genética
Neoplasias do Plexo Corióideo/patologia
Plexo Corióideo/patologia
Proteínas Proto-Oncogênicas c-myc/genética
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Animais
Carcinogênese/genética
Carcinogênese/patologia
Proliferação Celular
Dano ao DNA
Modelos Animais de Doenças
Seres Humanos
Camundongos
Camundongos Transgênicos
Mutação
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-myc); 0 (Tumor Suppressor Protein p53)
[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:180118
[St] Status:MEDLINE


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[PMID]:29441916
[Au] Autor:Fan X; Wang P; Sun Y; Jiang J; Du H; Wang Z; Duan Z; Lei H; Li H
[Ti] Título:Oleanolic acid derivatives inhibit the Wnt/ß-catenin signaling pathway by promoting the phosphorylation of ß-catenin in human SMMC-7721 cells.
[So] Source:Pharmazie;71(7):398-401, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Oleanolic acid, isolated from privet, has shown antitumor effects in several cancers. However, the underlying molecular mechanism associated with these effects is largely unknown. In this study, we explored the effect of oleanolic acid derivatives on the Wnt/ß-catenin signaling pathway in human hepatocellular carcinoma SMMC-7721 cells. The mRNA and protein levels of related genes were determined by real-time quantitative PCR and Western blot, respectively. Treatment of SMMC-7721 cells with oleanolic acid derivatives led to the downregulation of the mRNA and protein levels of ß-catenin, c-myc, and cyclin D1. Treatment with oleanolic acid derivatives decreased the levels of ß-catenin in both the cytoplasm and the nucleus. Moreover, oleanolic acid derivatives promoted the phosphorylation of ß-catenin (Ser33/37/Thr41) in the cytoplasm. Our results suggest that oleanolic acid derivatives inhibit the Wnt/ß-catenin signaling pathway by stimulating the phosphorylation of ß-catenin (Ser33/37/Thr41) in human SMMC-7721 cells.
[Mh] Termos MeSH primário: Ácido Oleanólico/análogos & derivados
Ácido Oleanólico/farmacologia
Via de Sinalização Wnt/efeitos dos fármacos
beta Catenina/efeitos dos fármacos
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Núcleo Celular/efeitos dos fármacos
Núcleo Celular/metabolismo
Ciclina D1/antagonistas & inibidores
Ciclina D1/biossíntese
Citoplasma/efeitos dos fármacos
Citoplasma/metabolismo
Regulação para Baixo/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-myc/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-myc/biossíntese
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CTNNB1 protein, human); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, Messenger); 0 (beta Catenin); 136601-57-5 (Cyclin D1); 6SMK8R7TGJ (Oleanolic Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6536


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[PMID]:28903484
[Au] Autor:Yang Y; Gao X; Zhang M; Yan S; Sun C; Xiao F; Huang N; Yang X; Zhao K; Zhou H; Huang S; Xie B; Zhang N
[Ad] Endereço:Department of Neurosurgery, The 1st Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong Province, PR China; Guangdong Provincial Key Laboratory of Pituitary Tumor, Guangzhou, Guangdong Province, PR China; Department of Scientific Research Section, The 1st Affiliated Hospital of Sun Y
[Ti] Título:Novel Role of FBXW7 Circular RNA in Repressing Glioma Tumorigenesis.
[So] Source:J Natl Cancer Inst;110(3), 2018 Mar 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Circular RNAs (circRNAs) are RNA transcripts that are widespread in the eukaryotic genome. Recent evidence indicates that circRNAs play important roles in tissue development, gene regulation, and carcinogenesis. However, whether circRNAs encode functional proteins remains elusive, although translation of several circRNAs was recently reported. Methods: CircRNA deep sequencing was performed by using 10 pathologically diagnosed glioblastoma samples and their paired adjacent normal brain tissues. Northern blotting, Sanger sequencing, antibody, and liquid chromatograph Tandem Mass Spectrometer were used to confirm the existence of circ-FBXW7 and its encoded protein in in two cell lines. Lentivirus-transfected stable U251 and U373 cells were used to assess the biological functions of the novel protein invitro and invivo (five mice per group). Clinical implications of circ-FBXW7 were assessed in 38 pathologically diagnosed glioblastoma samples and their paired periphery normal brain tissues by using quantitative polymerase chain reaction (two-sided log-rank test). Results: Circ-FBXW7 is abundantly expressed in the normal human brain (reads per kilobase per million mapped reads [RPKM] = 9.31). The spanning junction open reading frame in circ-FBXW7 driven by internal ribosome entry site encodes a novel 21-kDa protein, which we termed FBXW7-185aa. Upregulation of FBXW7-185aa in cancer cells inhibited proliferation and cell cycle acceleration, while knockdown of FBXW7-185aa promoted malignant phenotypes invitro and invivo. FBXW7-185aa reduced the half-life of c-Myc by antagonizing USP28-induced c-Myc stabilization. Moreover, circ-FBXW7 and FBXW7-185aa levels were reduced in glioblastoma clinical samples compared with their paired tumor-adjacent tissues (P < .001). Circ-FBXW7 expression positively associated with glioblastoma patient overall survival (P = .03). Conclusions: Endogenous circRNA encodes a functional protein in human cells, and circ-FBXW7 and FBXW7-185aa have potential prognostic implications in brain cancer.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/genética
Proteínas de Ciclo Celular/genética
Transformação Celular Neoplásica/genética
Proteínas F-Box/genética
Glioblastoma/genética
RNA/análise
Ubiquitina-Proteína Ligases/genética
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Neoplasias Encefálicas/química
Ciclo Celular/genética
Proteínas de Ciclo Celular/análise
Linhagem Celular Tumoral
Proliferação Celular/genética
Proteínas F-Box/análise
Proteína 7 com Repetições F-Box-WD
Feminino
Glioblastoma/química
Meia-Vida
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Transplante de Neoplasias
Fases de Leitura Aberta
Proteínas Proto-Oncogênicas c-myc/metabolismo
Análise de Sequência de RNA
Taxa de Sobrevida
Ubiquitina Tiolesterase/metabolismo
Ubiquitina-Proteína Ligases/análise
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (F-Box Proteins); 0 (F-Box-WD Repeat-Containing Protein 7); 0 (FBXW7 protein, human); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, circular); 63231-63-0 (RNA); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.1.2.15 (USP28 protein, human); EC 3.4.19.12 (Ubiquitin Thiolesterase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx166


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[PMID]:29295989
[Au] Autor:Gibori H; Eliyahu S; Krivitsky A; Ben-Shushan D; Epshtein Y; Tiram G; Blau R; Ofek P; Lee JS; Ruppin E; Landsman L; Barshack I; Golan T; Merquiol E; Blum G; Satchi-Fainaro R
[Ad] Endereço:Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, 69978, Israel.
[Ti] Título:Amphiphilic nanocarrier-induced modulation of PLK1 and miR-34a leads to improved therapeutic response in pancreatic cancer.
[So] Source:Nat Commun;9(1):16, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The heterogeneity of pancreatic ductal adenocarcinoma (PDAC) suggests that successful treatment might rely on simultaneous targeting of multiple genes, which can be achieved by RNA interference-based therapeutic strategies. Here we show a potent combination of microRNA and siRNA delivered by an efficient nanocarrier to PDAC tumors. Using proteomic-microRNA profiles and survival data of PDAC patients from TCGA, we found a novel signature for prolonged survival. Accordingly, we used a microRNA-mimic to increase miR-34a together with siRNA to silence PLK1 oncogene. For in vivo dual-targeting of this combination, we developed a biodegradable amphiphilic polyglutamate amine polymeric nanocarrier (APA). APA-miRNA-siRNA polyplexes systemically administered to orthotopically inoculated PDAC-bearing mice showed no toxicity and accumulated at the tumor, resulting in an enhanced antitumor effect due to inhibition of MYC oncogene, a common target of both miR-34a and PLK1. Taken together, our findings warrant this unique combined polyplex's potential as a novel nanotherapeutic for PDAC.
[Mh] Termos MeSH primário: Carcinoma Ductal Pancreático/genética
Proteínas de Ciclo Celular/genética
Regulação Neoplásica da Expressão Gênica
MicroRNAs/genética
Neoplasias Pancreáticas/genética
Proteínas Serina-Treonina Quinases/genética
Proteínas Proto-Oncogênicas/genética
RNA Interferente Pequeno/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Carcinoma Ductal Pancreático/metabolismo
Carcinoma Ductal Pancreático/terapia
Proteínas de Ciclo Celular/metabolismo
Linhagem Celular Tumoral
Portadores de Fármacos/química
Feminino
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas
Estimativa de Kaplan-Meier
Masculino
Camundongos Endogâmicos C57BL
Camundongos SCID
Meia-Idade
Nanoestruturas/química
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/terapia
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Proto-Oncogênicas/metabolismo
Proteínas Proto-Oncogênicas c-myc/genética
Proteínas Proto-Oncogênicas c-myc/metabolismo
Interferência de RNA
RNA Interferente Pequeno/química
Terapêutica com RNAi/métodos
Ensaios Antitumorais Modelo de Xenoenxerto/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Drug Carriers); 0 (MIRN34 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, Small Interfering); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (polo-like kinase 1)
[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:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02283-9


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[PMID]:28460446
[Au] Autor:Kapil S; Sharma BK; Patil M; Elattar S; Yuan J; Hou SX; Kolhe R; Satyanarayana A
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Molecular Oncology & Biomarkers Program, Georgia Cancer Center, Augusta University, Augusta, GA 30912, USA.
[Ti] Título:The cell polarity protein Scrib functions as a tumor suppressor in liver cancer.
[So] Source:Oncotarget;8(16):26515-26531, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Scrib is a membrane protein that is involved in the maintenance of apical-basal cell polarity of the epithelial tissues. However, Scrib has also been shown to be mislocalized to the cytoplasm in breast and prostate cancer. Here, for the first time, we report that Scrib not only translocates to the cytoplasm but also to the nucleus in hepatocellular carcinoma (HCC) cells, and in mouse and human liver tumor samples. We demonstrate that Scrib overexpression suppresses the growth of HCC cells in vitro, and Scrib deficiency enhances liver tumor growth in vivo. At the molecular level, we have identified the existence of a positive feed-back loop between Yap1 and c-Myc in HCC cells, which Scrib disrupts by simultaneously regulating the MAPK/ERK and Hippo signaling pathways. Overall, Scrib inhibits liver cancer cell proliferation by suppressing the expression of three oncogenes, Yap1, c-Myc and cyclin D1, thereby functioning as a tumor suppressor in liver cancer.
[Mh] Termos MeSH primário: Neoplasias Hepáticas/metabolismo
Proteínas de Membrana/metabolismo
Proteínas Supressoras de Tumor/metabolismo
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Proteínas Adaptadoras de Transdução de Sinal/genética
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Ciclo Celular/genética
Linhagem Celular Tumoral
Proliferação Celular
Transformação Celular Neoplásica/induzido quimicamente
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Ciclina D1/genética
Ciclina D1/metabolismo
Modelos Animais de Doenças
Expressão Gênica
Xenoenxertos
Seres Humanos
Neoplasias Hepáticas/genética
Sistema de Sinalização das MAP Quinases
Proteínas de Membrana/genética
Camundongos
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Ligação Proteica
Transporte Proteico
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Proto-Oncogênicas c-myc/genética
Proteínas Proto-Oncogênicas c-myc/metabolismo
Transdução de Sinais
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Membrane Proteins); 0 (Phosphoproteins); 0 (Proto-Oncogene Proteins c-myc); 0 (SCRIB protein, human); 0 (Tumor Suppressor Proteins); 0 (YAP1 (Yes-associated) protein, human); 136601-57-5 (Cyclin D1); EC 2.7.11.1 (Hippo protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15713


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[PMID]:29335202
[Au] Autor:Wei ZZ; Qin QP; Meng T; Deng CX; Liang H; Chen ZF
[Ad] Endereço:State Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmacy, Guangxi Normal University, 15 Yucai Road, Guilin 541004, PR China.
[Ti] Título:5-Bromo-oxoisoaporphine platinum(II) complexes exhibit tumor cell cytotoxcicity via inhibition of telomerase activity and disruption of c-myc G-quadruplex DNA and mitochondrial functions.
[So] Source:Eur J Med Chem;145:360-369, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Two platinum(II) complexes [Pt(L)(DMSO)Cl] (1) and [Pt(L)(pn)]Cl (2) with 5-bromo-oxoisoaporphine (H-L) were synthesized. We found that the two new platinum(II) complexes were more selective for Hep-G2 tumor cells than for normal cells (HL-7702, WI-38 and L-o2 cell lines). 5-Bromine-oxoisoaporphine platinum(II) complex 2 was a telomerase inhibitor targeting c-myc G4, and it triggered Hep-G2 cell apoptosis more potently than complex 1. Moreover, they induced cell apoptosis via disruption of mitochondrial functions. Significantly increased ROS level, loss of Δψ, decrease of bcl-2 level, and increase of some of the mitochondria-initiated apoptosis protein levels (including bax, Cyt C, caspase-3, caspase-9, and apaf-1) were observed in Hep-G2 cells. In brief, complexes 1 and 2 triggered Hep-G2 cell apoptosis mainly through inhibiting telomerase activity by interacting with c-myc promoter elements and disruption of mitochondrial pathway. Our results also showed the effects of second ligands on the in vitro antitumor activity in the order of pn > Cl and DMSO.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Quadruplex G/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Compostos Organoplatínicos/farmacologia
Proteínas Proto-Oncogênicas c-myc/antagonistas & inibidores
Telomerase/antagonistas & inibidores
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Mitocôndrias/metabolismo
Estrutura Molecular
Compostos Organoplatínicos/síntese química
Compostos Organoplatínicos/química
Proteínas Proto-Oncogênicas c-myc/metabolismo
Relação Estrutura-Atividade
Telomerase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Organoplatinum Compounds); 0 (Proto-Oncogene Proteins c-myc); EC 2.7.7.49 (Telomerase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


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[PMID]:29289266
[Au] Autor:Trop-Steinberg S; Azar Y
[Ad] Endereço:Faculty of Life and Health Sciences (ST-S), JCT Lev Academic Institute, Jerusalem, Israel. Electronic address: shivtia@g.jct.ac.il.
[Ti] Título:Is Myc an Important Biomarker? Myc Expression in Immune Disorders and Cancer.
[So] Source:Am J Med Sci;355(1):67-75, 2018 Jan.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The proto-oncogene Myc serves as a paradigm for understanding the dynamics of transcriptional regulation. Myc protein has been linked to immune dysfunction, cancer development and neoplastic transformation. We review recent research regarding functions of Myc as an important modulator in immune disorders, postallogeneic hematopoietic stem cell transplantation (HSCT) and several cancers. Myc overexpression has been repeatedly linked to immune disorders and specific cancers, such as myasthenia gravis, psoriasis, pemphigus vulgaris, atherosclerosis, long-term allogeneic survival among HSCT patients, (primary) inflammatory breast cancer, (primary) ovarian carcinoma and hematological malignancies: acute myeloid leukemia, chronic myelogenous leukemia, Hodgkin's lymphoma and diffuse large B-cell lymphoma. However, decreased expression of Myc has been observed in HSCT patients who did not survive. Understanding impaired or inappropriate expression of Myc may present a path for the discovery of new targets for therapeutic applications.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/biossíntese
Regulação Neoplásica da Expressão Gênica
Doenças do Sistema Imune/metabolismo
Neoplasias/metabolismo
Proteínas Proto-Oncogênicas c-myc/biossíntese
[Mh] Termos MeSH secundário: Aloenxertos
Intervalo Livre de Doença
Transplante de Células-Tronco Hematopoéticas
Seres Humanos
Doenças do Sistema Imune/patologia
Doenças do Sistema Imune/terapia
Neoplasias/patologia
Neoplasias/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (MYC protein, human); 0 (Proto-Oncogene Proteins c-myc)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180101
[St] Status:MEDLINE


  9 / 10424 MEDLINE  
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[PMID]:28464854
[Au] Autor:Chi L; Zou Y; Qin L; Ma W; Hao Y; Tang Y; Luo R; Wu Z
[Ad] Endereço:Cancer Center, TCM-Integrated Hospital, Southern Medical University, Guangzhou, 510315, China.
[Ti] Título:TIMELESS contributes to the progression of breast cancer through activation of MYC.
[So] Source:Breast Cancer Res;19(1):53, 2017 May 02.
[Is] ISSN:1465-542X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Breast cancer is the most common malignancy and the leading cause of cancer death among women. TIMELESS (TIM), a circadian rhythm regulator, has been recently implicated in the progression of human cancer. However, the role of TIM in the progression of breast cancer has not been well-characterized. METHODS: Immunohistochemistry (IHC) staining was used to examine TIM levels in breast cancer specimens. Mammosphere formation analysis and side population analysis were used to examine the effect of TIM on the self-renewal of breast cancer stem cells. A wound healing assay and a Transwell assay were used to determine the role of TIM in breast cancer cell migration and invasion. A soft agar growth assay in vitro and tumorigenicity in vivo were used to determine the role of TIM in tumorigenicity. RESULTS: TIM levels in both breast cancer cell lines and tissues were significantly upregulated. Patients with high TIM had poorer prognosis than patients with low TIM. Overexpression of TIM dramatically enhanced, while knockdown of TIM suppressed the self-renewal of cancer stem cells (CSCs), cell invasion and migration abilities of breast cancer cells in vitro. Moreover, overexpression of TIM significantly augmented, while knockdown of TIM reduced the tumorigenicity of breast cancer cells in vivo. Mechanism studies revealed that TIM upregulated the expression and the trans-activity of the well-known oncogene MYC. Inhibition of MYC significantly blocked the effects of TIM on CSC population, cell invasion and anchor-independent cell growth. CONCLUSION: TIM plays an important role in promoting breast cancer progression and may represent a novel therapeutic target for breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Proteínas de Ciclo Celular/genética
Proliferação Celular/genética
Peptídeos e Proteínas de Sinalização Intracelular/genética
Proteínas Proto-Oncogênicas c-myc/genética
[Mh] Termos MeSH secundário: Neoplasias da Mama/patologia
Progressão da Doença
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Células MCF-7
Invasividade Neoplásica/genética
Células-Tronco Neoplásicas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Intracellular Signaling Peptides and Proteins); 0 (MYC protein, human); 0 (Proto-Oncogene Proteins c-myc); 0 (TIMELESS protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s13058-017-0838-1


  10 / 10424 MEDLINE  
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[PMID]:29248874
[Au] Autor:Ma J; Li Y; Wu M; Li X
[Ad] Endereço:College of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.
[Ti] Título:Oxidative stress-mediated p53/p21 pathway may be involved in microcystin-LR-induced cytotoxicity in HepG2 cells.
[So] Source:Chemosphere;194:773-783, 2018 Mar.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A previous study showed that microcystin-LR (MC-LR) exerted cytotoxicity and induced apoptosis in HepG2 cells. In the present study, we investigated whether oxidative stress-mediated p53/p21 is involved in this process to further elucidate the mechanism of cytotoxicity induced by MC-LR. Morphological evaluation showed that MC-LR induced time- and dose-dependent cytotoxicity in HepG2 cells. Biochemical assays revealed that MC-LR exposure altered the protein levels of HSP70 and HSP90, generally inhibited superoxide dismutase and catalase, reduced glutathione content, and increased the cellular malondialdehyde level of HepG2 cells, suggesting that MC-LR may induce biochemical disturbance and oxidative stress in HepG2 cells. The protein levels of p-p53 and p21 were markedly increased by MC-LR exposure in a concentration-dependent manner, suggesting that p53 and p21 may be involved in the process. Moreover, we also found that the proto-oncogene c-myc was significantly activated in HepG2 cells following MC-LR exposure, indicating that c-myc in HepG2 cells was potentially involved in response to MC-LR-induced apoptosis. These findings may contribute to further understanding the in vitro molecular mechanism of MC-LR hepatotoxicity.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Microcistinas/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Catalase/metabolismo
Glutationa/metabolismo
Células Hep G2
Seres Humanos
Malondialdeído/metabolismo
Proteínas Proto-Oncogênicas c-myc/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN1A protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (MYC protein, human); 0 (Microcystins); 0 (Proto-Oncogene Proteins c-myc); 0 (Tumor Suppressor Protein p53); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase); EQ8332842Y (cyanoginosin LR); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE



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