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  1 / 230434 MEDLINE  
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[PMID]:28747142
[Au] Autor:Zhao Y; Stepto H; Schneider CK
[Ad] Endereço:1 Division of Advanced Therapies, National Institute for Biological Standards and Control (NIBSC) , Medicines and Health Products Regulatory Agency (MHRA), South Mimms, United Kingdom .
[Ti] Título:Development of the First World Health Organization Lentiviral Vector Standard: Toward the Production Control and Standardization of Lentivirus-Based Gene Therapy Products.
[So] Source:Hum Gene Ther Methods;28(4):205-214, 2017 08.
[Is] ISSN:1946-6544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gene therapy is a rapidly evolving field. So far, there have been >2,400 gene therapy products in clinical trials and four products on the market. A prerequisite for producing gene therapy products is ensuring their quality and safety. This requires appropriately controlled and standardized production and testing procedures that result in consistent safety and efficacy. Assuring the quality and safety of lentivirus-based gene therapy products in particular presents a great challenge because they are cell-based multigene products that include viral and therapeutic proteins as well as modified cells. In addition to the continuous refinement of a product, changes in production sites and manufacturing processes have become more and more common, posing challenges to developers regarding reproducibility and comparability of results. This paper discusses the concept of developing a first World Health Organization International Standard, suitable for the standardization of assays and enabling comparison of cross-trial and cross-manufacturing results for this important vector platform. The standard will be expected to optimize the development of gene therapy medicinal products, which is especially important, given the usually orphan nature of the diseases to be treated, naturally hampering reproducibility and comparability of results.
[Mh] Termos MeSH primário: Terapia Genética/normas
Vetores Genéticos/normas
Lentivirus/genética
Organização Mundial da Saúde
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Terapia Genética/métodos
Vetores Genéticos/genética
Células HEK293
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180310
[Lr] Data última revisão:
180310
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1089/hgtb.2017.078


  2 / 230434 MEDLINE  
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[PMID]:29482389
[Au] Autor:Elzahabi HSA; Nossier ES; Khalifa NM; Alasfoury RA; El-Manawaty MA
[Ad] Endereço:a Department of Pharmaceutical Chemistry , Faculty of Pharmacy (Girls), Al-Azhar University , Cairo , Egypt.
[Ti] Título:Anticancer evaluation and molecular modeling of multi-targeted kinase inhibitors based pyrido[2,3-d]pyrimidine scaffold.
[So] Source:J Enzyme Inhib Med Chem;33(1):546-557, 2018 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:An efficient synthesis of substituted pyrido[2,3-d]pyrimidines was carried out and evaluated for in vitro anticancer activity against five cancer cell lines, namely hepatic cancer (HepG-2), prostate cancer (PC-3), colon cancer (HCT-116), breast cancer (MCF-7), and lung cancer (A-549) cell lines. Regarding HepG-2, PC-3, HCT-116 cancer cell lines, 7-(4-chlorophenyl)-2-(3-methyl-5-oxo-2,3-dihydro-1H-pyrazol-1-yl)-5-(p-tolyl)- pyrido[2,3-d]pyrimidin-4(3H)-one (5a) exhibited strong, more potent anticancer (IC : 0.3, 6.6 and 7 µM) relative to the standard doxorubicin (IC : 0.6, 6.8 and 12.8 µM), respectively. Kinase inhibitory assessment of 5a showed promising inhibitory activity against three kinases namely PDGFR ß, EGFR, and CDK4/cyclin D1 at two concentrations 50 and 100 µM in single measurements. Further, a molecular docking study for compound 5a was performed to verify the binding mode towards the EGFR and CDK4/cyclin D1 kinases.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Quinase 4 Dependente de Ciclina/antagonistas & inibidores
Inibidores de Proteínas Quinases/farmacologia
Piridinas/farmacologia
Pirimidinas/farmacologia
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Receptor beta de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Quinase 4 Dependente de Ciclina/metabolismo
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Modelos Moleculares
Estrutura Molecular
Inibidores de Proteínas Quinases/síntese química
Inibidores de Proteínas Quinases/química
Piridinas/síntese química
Piridinas/química
Pirimidinas/síntese química
Pirimidinas/química
Receptor do Fator de Crescimento Epidérmico/metabolismo
Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); 0 (Pyridines); 0 (Pyrimidines); 0 (pyrido(3,2-d)pyrimidine); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta); EC 2.7.11.22 (CDK4 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 4)
[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:180228
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2018.1437729


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[PMID]:29455234
[Au] Autor:Wang S; Wang X; Liu M; Bai O
[Ad] Endereço:Department of Hematology, The First Hospital of Jilin University, No. 71 Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
[Ti] Título:Blastic plasmacytoid dendritic cell neoplasm: update on therapy especially novel agents.
[So] Source:Ann Hematol;97(4):563-572, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematopoietic malignancy mainly affecting elderly patients. Most patients present with asymptomatic skin lesions as the first symptom and has a high frequency of bone marrow involvement. BPDCN is typically characterized by CD4+ and CD 56+ co-expression without common lymphoid or myeloid lineage markers. There is no consensus on the optimal therapeutic strategy for BPDCN. It is highly responsive to chemotherapy but the median event-free survival is very short. Allogeneic stem cell transplantation may improve the prognosis of BPDCN but the rate of relapse is still high. There are no specific targeted agents approved for patients with BPDCN, but advances in the understanding of the pathobiology of BPDCN and the results of early clinical studies have revealed novel targets and potentially effective agents. Novel targeted therapies may improve outcomes for patients with BPDCN in the future.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Células Dendríticas/efeitos dos fármacos
Drogas em Investigação/uso terapêutico
Neoplasias Hematológicas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Linhagem Celular Tumoral
Neoplasias do Sistema Nervoso Central/diagnóstico
Neoplasias do Sistema Nervoso Central/prevenção & controle
Neoplasias do Sistema Nervoso Central/secundário
Células Dendríticas/patologia
Drogas em Investigação/farmacologia
Neoplasias Hematológicas/diagnóstico
Neoplasias Hematológicas/patologia
Neoplasias Hematológicas/cirurgia
Transplante de Células-Tronco Hematopoéticas/efeitos adversos
Seres Humanos
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drugs, Investigational)
[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:180219
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-018-3259-z


  4 / 230434 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


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[PMID]:29414979
[Au] Autor:Takahashi H; Kozhuharova A; Sharma H; Hirose M; Ohyama T; Fasolo F; Yamazaki T; Cotella D; Santoro C; Zucchelli S; Gustincich S; Carninci P
[Ad] Endereço:RIKEN Center for Life Science Technologies, Division of Genomic Technologies, Yokohama, Kanagawa, Japan.
[Ti] Título:Identification of functional features of synthetic SINEUPs, antisense lncRNAs that specifically enhance protein translation.
[So] Source:PLoS One;13(2):e0183229, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:SINEUPs are antisense long noncoding RNAs, in which an embedded SINE B2 element UP-regulates translation of partially overlapping target sense mRNAs. SINEUPs contain two functional domains. First, the binding domain (BD) is located in the region antisense to the target, providing specific targeting to the overlapping mRNA. Second, the inverted SINE B2 represents the effector domain (ED) and enhances translation. To adapt SINEUP technology to a broader number of targets, we took advantage of a high-throughput, semi-automated imaging system to optimize synthetic SINEUP BD and ED design in HEK293T cell lines. Using SINEUP-GFP as a model SINEUP, we extensively screened variants of the BD to map features needed for optimal design. We found that most active SINEUPs overlap an AUG-Kozak sequence. Moreover, we report our screening of the inverted SINE B2 sequence to identify active sub-domains and map the length of the minimal active ED. Our synthetic SINEUP-GFP screening of both BDs and EDs constitutes a broad test with flexible applications to any target gene of interest.
[Mh] Termos MeSH primário: Biossíntese de Proteínas/genética
Proteínas/genética
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Células HEK293
Seres Humanos
Camundongos
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proteins); 0 (RNA, Long Noncoding)
[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:180208
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183229


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[PMID]:29408622
[Au] Autor:Zeng Y; Shen Z; Gu W; Wu M
[Ad] Endereço:Department of Medical Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu 210009, China; The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, China. Ele
[Ti] Título:Inhibition of hepatocellular carcinoma tumorigenesis by curcumin may be associated with CDKN1A and CTGF.
[So] Source:Gene;651:183-193, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This study aimed to explore crucial genes, transcription factors (TFs), and microRNAs (miRNAs) associated with the effects of curcumin against hepatocellular carcinoma (HCC). We downloaded data (GSE59713) from Gene Expression Omnibus to analyze differentially expressed genes (DEGs) between curcumin-treated and untreated HCC cell lines. Then, we identified the disease ontology (DO) and functional enrichment analysis of these DEGs and analyzed their protein-protein interactions (PPIs). Additionally, we constructed TF-target gene and miRNA-target gene regulatory networks and explored the potential functions of these DEGs. Finally, we detected the expression of CDKN1A, CTGF, LEF1 TF and MIR-19A regulated by curcumin in PLC/PRF/5 cells using RT-PCR. In total, 345 upregulated and 212 downregulated genes were identified. The main enriched pathway of upregulated genes was the TNF signaling pathway. The downregulated genes were significantly enriched in TGF-beta signaling pathway. In addition, most DEGs were significantly enriched in DO terms such as liver cirrhosis, hepatitis, hepatitis C and cholestasis (eg., CTGF). In the constructed PPI network, CDKN1A and CTGF were the key proteins. Moreover, LEF1, CDKN1A, and miR-19A that regulated CTGF were highlighted in the regulatory networks. Furthermore, the expression of CDKN1A, CTGF, LEF1 TF and miR-19A regulated by curcumin in PLC/PRF/5 cells was consistent with the aforementioned bioinformatics analysis results. To conclude, curcumin might exert its protective effects against HCC tumorigenesis by downregulating LEF1 and downregulating CTGF regulated by MIR-19A and upregulating CDKN1A expression.
[Mh] Termos MeSH primário: Carcinogênese/efeitos dos fármacos
Carcinoma Hepatocelular/tratamento farmacológico
Fator de Crescimento do Tecido Conjuntivo/genética
Curcumina/uso terapêutico
Inibidor de Quinase Dependente de Ciclina p21/genética
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/genética
Linhagem Celular Tumoral
Bases de Dados Genéticas
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Neoplasias Hepáticas/genética
Fator 1 de Ligação ao Facilitador Linfoide/genética
MicroRNAs/genética
Proteínas de Neoplasias/genética
Mapas de Interação de Proteínas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN1A protein, human); 0 (CTGF protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (LEF1 protein, human); 0 (Lymphoid Enhancer-Binding Factor 1); 0 (MIRN19 microRNA, human); 0 (MicroRNAs); 0 (Neoplasm Proteins); 139568-91-5 (Connective Tissue Growth Factor); IT942ZTH98 (Curcumin)
[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


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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]:29377903
[Au] Autor:Koldehoff M; Lindemann M; Ross SR; Elmaagacli AH
[Ad] Endereço:Department of Bone Marrow Transplantation, West German Cancer Center, University Hospital of Essen, Essen, Germany.
[Ti] Título:Cytomegalovirus induces HLA-class-II-restricted alloreactivity in an acute myeloid leukemia cell line.
[So] Source:PLoS One;13(1):e0191482, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cytomegalovirus (HCMV) reactivation is found frequently after allogeneic hematopoietic stem cell transplantation (alloSCT) and is associated with an increased treatment-related mortality. Recent reports suggest a link between HCMV and a reduced risk of cancer progression in patients with acute leukemia or lymphoma after alloSCT. Here we show that HCMV can inhibit the proliferation of the acute myeloid leukemia cell line Kasumi-1 and the promyeloid leukemia cell line NB4. HCMV induced a significant up-regulation of HLA-class-II-molecules, especially HLA-DR expression and an increase of apoptosis, granzyme B, perforin and IFN-γ secretion in Kasumi-1 cells cocultured with peripheral blood mononuclear cells (PBMCs). Indolamin-2,3-dioxygenase on the other hand led only to a significant dose-dependent effect on IFN-γ secretion without effects on proliferation. The addition of CpG-rich oligonucleotides and ganciclovir reversed those antiproliferative effects. We conclude that HCMV can enhance alloreactivity of PBMCs against Kasumi-1 and NB4 cells in vitro. To determine if this phenomenon may be clinically relevant further investigations will be required.
[Mh] Termos MeSH primário: Antígenos de Histocompatibilidade Classe II/imunologia
Leucemia Mieloide Aguda/imunologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Técnicas de Cocultura
Seres Humanos
Leucemia Mieloide Aguda/terapia
Leucemia Mieloide Aguda/virologia
Transplante de Células-Tronco
Transplante Homólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Histocompatibility Antigens Class II)
[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:180130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191482


  9 / 230434 MEDLINE  
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[PMID]:29366479
[Au] Autor:Xia E; Bhandari A; Shen Y; Zhou X; Sindan N; Xiang J; Guan Y; Yang F; Wang O
[Ad] Endereço:Department of Thyroid & Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, PR China.
[Ti] Título:LncRNA CCND2-AS1 promotes proliferation, migration, and invasion in papillary thyroid carcinoma.
[So] Source:Biochem Biophys Res Commun;496(2):628-632, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In decades, a lot of long non-coding RNAs (LncRNAs) have been proven to exert influences on tumorigenesis in vitro and in vivo. Many lncRNAs have been reported as effective therapeutic targets and biomarkers in various cancers. However, whether LncRNAs are associated with the progression of PTC remains largely unknown. In this study, we measured the expression of CCND2-AS1 in PTC cell lines by quantitative real-time polymerase chain reaction (qRT-PCR).We found that CCND2-AS1 expression was significantly over-expressed in PTC cell lines compared to normal thyroid epithelial cells. Gain-and loss-of-function experiments were performed to investigate the role of CCND2-AS1 in PTC cells. In vitro experiments, we proved that CCND2-AS1 knockdown in TPC1 significantly suppressed cell proliferation, migration, and invasion, while CCND2-AS1 overexpression in BCPAP had the opposite effects. Meanwhile, we also found that CCND2-AS1 could regulate N-cadherin and Vimentin expression, which may influence invasion and migration. Our findings indicate that the lncRNA CCND2-AS1 is a gene associated with PTC and might become a potential therapeutic target.
[Mh] Termos MeSH primário: Carcinoma Papilar/genética
Regulação Neoplásica da Expressão Gênica
Invasividade Neoplásica/genética
RNA Longo não Codificante/genética
Neoplasias da Glândula Tireoide/genética
[Mh] Termos MeSH secundário: Carcinoma Papilar/patologia
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Seres Humanos
Invasividade Neoplásica/patologia
Glândula Tireoide/patologia
Neoplasias da Glândula Tireoide/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Long Noncoding)
[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:180126
[St] Status:MEDLINE


  10 / 230434 MEDLINE  
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[PMID]:29364966
[Au] Autor:Maleki Vareki S; Salim KY; Danter WR; Koropatnick J
[Ad] Endereço:Cancer Research Laboratory Program, Lawson Health Research Institute, London, Ontario, Canada.
[Ti] Título:Novel anti-cancer drug COTI-2 synergizes with therapeutic agents and does not induce resistance or exhibit cross-resistance in human cancer cell lines.
[So] Source:PLoS One;13(1):e0191766, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Emerging drug-resistance and drug-associated toxicities are two major factors limiting successful cancer therapy. Combinations of chemotherapeutic drugs have been used in the clinic to improve patient outcome. However, cancer cells can acquire resistance to drugs, alone or in combination. Resistant tumors can also exhibit cross-resistance to other chemotherapeutic agents, resulting in sub-optimal treatment and/or treatment failure. Therefore, developing novel oncology drugs that induce no or little acquired resistance and with a favorable safety profile is essential. We show here that combining COTI-2, a novel clinical stage agent, with multiple chemotherapeutic and targeted agents enhances the activity of these drugs in vitro and in vivo. Importantly, no overt toxicity was observed in the combination treatment groups in vivo. Furthermore, unlike the tested chemotherapeutic drugs, cancer cells did not develop resistance to COTI-2. Finally, some chemo-resistant tumor cell lines only showed mild cross-resistance to COTI-2 while most remained sensitive to it.
[Mh] Termos MeSH primário: Aminoquinolinas/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Tiossemicarbazonas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Carcinoma Pulmonar de Células não Pequenas/patologia
Linhagem Celular Tumoral
Cisplatino/administração & dosagem
Desoxicitidina/administração & dosagem
Desoxicitidina/análogos & derivados
Resistência a Medicamentos Antineoplásicos
Neoplasias Pulmonares/patologia
Camundongos
Paclitaxel/administração & dosagem
Vimblastina/administração & dosagem
Vimblastina/análogos & derivados
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (COTI-2 compound); 0 (Thiosemicarbazones); 0W860991D6 (Deoxycytidine); 5V9KLZ54CY (Vinblastine); B76N6SBZ8R (gemcitabine); P88XT4IS4D (Paclitaxel); Q20Q21Q62J (Cisplatin); Q6C979R91Y (vinorelbine)
[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:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191766



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