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[PMID]:29351307
[Au] Autor:Merentie M; Rissanen R; Lottonen-Raikaslehto L; Huusko J; Gurzeler E; Turunen MP; Holappa L; Mäkinen P; Ylä-Herttuala S
[Ad] Endereço:A. I. Virtanen Institute for Molecular Sciences, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland.
[Ti] Título:Doxycycline modulates VEGF-A expression: Failure of doxycycline-inducible lentivirus shRNA vector to knockdown VEGF-A expression in transgenic mice.
[So] Source:PLoS One;13(1):e0190981, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vascular endothelial growth factor-A (VEGF-A) is the master regulator of angiogenesis, vascular permeability and growth. However, its role in mature blood vessels is still not well understood. To better understand the role of VEGF-A in the adult vasculature, we generated a VEGF-A knockdown mouse model carrying a doxycycline (dox)-regulatable short hairpin RNA (shRNA) transgene, which silences VEGF-A. The aim was to find the critical level of VEGF-A reduction for vascular well-being in vivo. In vitro, the dox-inducible lentiviral shRNA vector decreased VEGF-A expression efficiently and dose-dependently in mouse endothelial cells and cardiomyocytes. In the generated transgenic mice plasma VEGF-A levels decreased shortly after the dox treatment but returned back to normal after two weeks. VEGF-A expression decreased shortly after the dox treatment only in some tissues. Surprisingly, increasing the dox exposure time and dose led to elevated VEGF-A expression in some tissues of both wildtype and knockdown mice, suggesting that dox itself has an effect on VEGF-A expression. When the effect of dox on VEGF-A levels was further tested in naïve/non-transduced cells, the dox administration led to a decreased VEGF-A expression in endothelial cells but to an increased expression in cardiomyocytes. In conclusion, the VEGF-A knockdown was achieved in a dox-regulatable fashion with a VEGF-A shRNA vector in vitro, but not in the knockdown mouse model in vivo. Dox itself was found to regulate VEGF-A expression explaining the unexpected results in mice. The effect of dox on VEGF-A levels might at least partly explain its previously reported beneficial effects on myocardial and brain ischemia. Also, this effect on VEGF-A should be taken into account in all studies using dox-regulated vectors.
[Mh] Termos MeSH primário: Doxiciclina/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Lentivirus/genética
RNA Interferente Pequeno/genética
Fator A de Crescimento do Endotélio Vascular/genética
[Mh] Termos MeSH secundário: Animais
Vetores Genéticos
Camundongos
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (Vascular Endothelial Growth Factor A); N12000U13O (Doxycycline)
[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:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190981


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[PMID]:28452703
[Au] Autor:Shin JM; Park JH; Kim HJ; Park IH; Lee HM
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Korea University College of Medicine, Seoul, South Korea.
[Ti] Título:Cigarette smoke extract increases vascular endothelial growth factor production TLR4/ROS/MAPKs/NF-kappaB pathway in nasal fibroblast.
[So] Source:Am J Rhinol Allergy;31(2):78-84, 2017 Mar 01.
[Is] ISSN:1945-8932
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Cigarette smoke is a complex mixture of various chemical compounds, including free radicals and highly toxic compounds. Cigarette smoke exposure has been shown to be associated with chronic rhinosinusitis and tissue remodeling in upper airway. Vascular endothelial growth factor (VEGF) is one of the cytokines with a crucial role in tissue remodeling of airway. The aims of this study were to determine the effects of cigarette smoke extract (CSE) on VEGF expression and to investigate the underlying molecular mechanisms of CSE in nasal fibroblasts. METHODS: Nasal fibroblasts were stimulated with CSE. Cytotoxicity was evaluated by 3-(4,5- dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay. The expression level of VEGF was measured using reverse transcription-polymerase chain reaction (RT-PCR), and enzyme-linked immunosorbent assay. Messenger RNA (mRNA) expression level of TLR4 were determined by RT-PCR. Small interfering RNA (siRNA) for TLR4 was transfected to suppress TLR4 expression. Activation of reactive oxygen species (ROS) was analyzed by using dichloro-dihydro-fluorescein diacetate assay. Mitogen-activated protein kinase (MAPK) and NF-kappaB activations were determined by using western blot and/or luciferase assay. RESULTS: CSE had no significant cytotoxic effect in nasal fibroblast up to 5%. CSE significantly increased both VEGF mRNA and protein expression dose-dependently. The down-regulation of TLR4 transcription by siRNA treatment suppressed CSE-induced expressions of both TLR4 and VEGF. Pretreatment with ROS scavengers, specific inhibitors of each MAPK, and NF-kappaB inhibitor significantly decreased CSE-induced VEGF expression. CONCLUSIONS: CSE has a stimulatory effect on VEGF expression through the TLR4, ROS, MAPK, and NF-kappaB signaling pathway in nasal fibroblasts.
[Mh] Termos MeSH primário: Fibroblastos/fisiologia
Nariz/patologia
Receptor 4 Toll-Like/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Mh] Termos MeSH secundário: Adulto
Morte Celular
Células Cultivadas
Fumar Cigarros/efeitos adversos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Regulação da Expressão Gênica
Seres Humanos
Masculino
NF-kappa B/metabolismo
RNA Interferente Pequeno/genética
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais
Receptor 4 Toll-Like/genética
Fator A de Crescimento do Endotélio Vascular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (TLR4 protein, human); 0 (Toll-Like Receptor 4); 0 (Vascular Endothelial Growth Factor A); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.2500/ajra.2017.31.4415


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[PMID]:28461099
[Au] Autor:Alaaeldin E; Abu Lila AS; Ando H; Fukushima M; Huang CL; Wada H; Sarhan HA; Khaled KA; Ishida T
[Ad] Endereço:Department of Pharmacokinetics and Biopharmaceutics, Institute of Biomedical Sciences, Tokushima University, 1-78-1, Sho-machi, Tokushima 770-8505, Japan; Department of Pharmaceutics, Faculty of Pharmacy, Minia University, Minia 61519, Egypt.
[Ti] Título:Co-administration of liposomal l-OHP and PEGylated TS shRNA-lipoplex: A novel approach to enhance anti-tumor efficacy and reduce the immunogenic response to RNAi molecules.
[So] Source:J Control Release;255:210-217, 2017 Jun 10.
[Is] ISSN:1873-4995
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Many therapeutic strategies have been applied in efforts to conquer the development and/or progression of cancer. The combination of chemotherapy and an RNAi-based approach has proven to be an efficient anticancer therapy. However, the feasibility of such a therapeutic strategy has been substantially restricted either by the failure to achieve the efficient delivery of RNAi molecules to tumor tissue or by the immunostimulatory response triggered by RNAi molecules. In this study, therefore, we intended to investigate the efficacy of using liposomal oxaliplatin (liposomal l-OHP) to guarantee the efficient delivery of RNAi molecules, namely shRNA against thymidylate synthase (TS shRNA) complexed with cationic liposome (TS shRNA-lipoplex), to solid tumors, and to suppress the immunostimulatory effect of RNAi molecules, TS shRNA, following intravenous administration. Herein, we describe how liposomal l-OHP enhanced the intra-tumor accumulation of TS shRNA-lipoplex and significantly reduced the immunostimulatory response triggered by TS shRNA. Consequently, such enhanced accumulation of TS shRNA-lipoplex along with the cytotoxic effect of liposomal l-OHP led to a remarkable tumor growth suppression (compared to mono-therapy) following systemic administration. Our results, therefore, may have important implications for the provision of a safer and more applicable combination therapy of RNAi molecules and anti-cancer agents that can produce a more reliable anti-tumor effect.
[Mh] Termos MeSH primário: Antineoplásicos/administração & dosagem
Neoplasias/terapia
Compostos Organoplatínicos/administração & dosagem
RNA Interferente Pequeno/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Antineoplásicos/farmacocinética
Antineoplásicos/uso terapêutico
Linhagem Celular Tumoral
Citocinas/metabolismo
Seres Humanos
Lipossomos
Masculino
Camundongos Endogâmicos BALB C
Camundongos Nus
Neoplasias/genética
Neoplasias/metabolismo
Compostos Organoplatínicos/química
Compostos Organoplatínicos/farmacocinética
Compostos Organoplatínicos/uso terapêutico
Polietilenoglicóis/química
Interferência de RNA
RNA Interferente Pequeno/química
RNA Interferente Pequeno/farmacocinética
RNA Interferente Pequeno/uso terapêutico
Timidilato Sintase/genética
Distribuição Tecidual
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cytokines); 0 (Liposomes); 0 (Organoplatinum Compounds); 0 (RNA, Small Interfering); 04ZR38536J (oxaliplatin); 30IQX730WE (Polyethylene Glycols); EC 2.1.1.45 (Thymidylate Synthase)
[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:170503
[St] Status:MEDLINE


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[PMID]:29429182
[Au] Autor:Niu JT; Liu SG; Huang YW; Li C
[Ad] Endereço:Department of Otorhinolaryngology Head and Neck Surgery, Second Hospital, Tianjin Medical University, Tianjin 300221, China.
[Ti] Título:[The effect of miR-497 on laryngeal squamous cell carcinoma invasion through modulating PlexinA4].
[So] Source:Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi;53(2):124-130, 2018 Feb 07.
[Is] ISSN:1673-0860
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To study the roles of miR-497 and PlexinA4 in the progression of laryngeal squamous cell carcinoma. The expressions of miR-497 and PlexinA4 in fresh tumor specimens and adjacent normal mucosa tissues as well as in cell lines of laryngeal squamous cell carcinoma (LSCC) were detected with qRT-PCR and immunohistochemistry. The association of miR-497 and PlexinA4 expressions with clinicopathologic factors and their prognostic values in LSCC were evaluated PlexinA4 siRNA and pcDNA3.1 (+ )/PlexinA4 plasmid were transfected into the LSCC and measured by Transwell to evaluate their effect on the invasion of LSCC. miR-497 was low expression in LSCC, which related to pathological differentiation, while PlexinA4 mRNA was high expression in LSCC. Kaplan-Meier method showed that the prognosis of patients with high miR-497 expression was better than that of patients with low miR-497 expression (χ(2)=10.342, =0.001); . Cox regression analysis showed that miR-497 was an independent prognostic factor for LSCC. The double luciferase reporter gene showed that the variation of the fluorescence activity of wild type PlexinA4 was significantly different from that of the control group ( <0.01). In Hep-2 and TU212 cell line, the number of cells with PlexinA4 siRNA passing through the compartments was 70.00±10.85 and 85.00±6.45, significantly higher than control ( values were 30.251 and 23.936, both <0.05), the number of cells with pcDNA3.1 (+ ) /PlexinA4 was 170.56±11.95 and 142.00±10.43, also significantly less than control (F values were 35.104 and 29.643, both <0.05). The expression of miR-497 in LSCC is decreased, indicating poor prognosis, which is as an independent risk factor for prognosis of LSCC. miR-497 may modulate LSCC invasion through PlexinA4.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/metabolismo
Neoplasias Laríngeas/metabolismo
MicroRNAs/metabolismo
Receptores de Superfície Celular/metabolismo
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/patologia
Proliferação Celular
Progressão da Doença
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Mucosa Laríngea/metabolismo
Neoplasias Laríngeas/mortalidade
Neoplasias Laríngeas/patologia
Prognóstico
RNA Interferente Pequeno
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN497 microRNA, human); 0 (MicroRNAs); 0 (Plxna4 protein, human); 0 (RNA, Small Interfering); 0 (Receptors, Cell Surface)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1673-0860.2018.02.008


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[PMID]:29190611
[Au] Autor:Liu J; Rao J; Lou X; Zhai J; Ni Z; Wang X
[Ad] Endereço:Department of Respiratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
[Ti] Título:Upregulated TRIM11 Exerts its Oncogenic Effects in Hepatocellular Carcinoma Through Inhibition of P53.
[So] Source:Cell Physiol Biochem;44(1):255-266, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The tripartite motif containing (TRIM) family plays crucial roles in tumor development and progression. However, little is known about the function and mechanism of TRIM11 in hepatocellular carcinoma (HCC). METHODS: The expression levels of TRIM11 were examined by real-time PCR, Western blot and Immunohistochemical (IHC) staining. TRIM11 knockdown cells were produced by lentivirus infection, and functional assays, such as MTT, colony formation assay, migration and invasion assays and a xenograft tumor model were used to investigate the role of TRIM11 in HCC. We also determined the effect of TRIM11 on p53 signaling and its downstream molecules. RESULTS: We found that TRIM11 mRNA and protein levels were significantly increased in HCC tissues as compared with normal tissues; increased levels correlated with poor patient survival. By loss- and gain-of-function investigations, knockdown of TRIM11 suppressed cell proliferation, migration, invasion in vitro and tumor growth in vivo. Moreover, TRIM11 negatively regulated p53 expression. Knockdown of p53 abrogated the in vitro and in vivo biological functions of TRIM11 shRNA in HCC cells. CONCLUSIONS: These data show that TRIM11 exerts its oncogenic effect in HCC by downregulating p53 both in vitro and in vivo. Our data provide new insights into the pathogenesis of HCC and indicate that TRIM11 may serve as a new therapeutic target for HCC treatment.
[Mh] Termos MeSH primário: Proteínas com Motivo Tripartido/genética
Proteínas com Motivo Tripartido/metabolismo
Proteína Supressora de Tumor p53/metabolismo
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Movimento Celular
Proliferação Celular
Ciclina D1/genética
Ciclina D1/metabolismo
Inibidor de Quinase Dependente de Ciclina p21/genética
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Inibidor de Quinase Dependente de Ciclina p27/genética
Inibidor de Quinase Dependente de Ciclina p27/metabolismo
Regulação para Baixo
Transição Epitelial-Mesenquimal
Células Hep G2
Seres Humanos
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Transplante Heterólogo
Proteínas com Motivo Tripartido/antagonistas & inibidores
Proteína Supressora de Tumor p53/antagonistas & inibidores
Proteína Supressora de Tumor p53/genética
Ubiquitina-Proteína Ligases/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (RNA, Small Interfering); 0 (TP53 protein, human); 0 (Tripartite Motif Proteins); 0 (Tumor Suppressor Protein p53); 136601-57-5 (Cyclin D1); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); EC 2.3.2.27 (TRIM11 protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1159/000484678


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[PMID]:28464292
[Au] Autor:Charbgoo F; Behmanesh M; Nikkhah M; Kane EG
[Ad] Endereço:Department of Nanobiotechnology, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
[Ti] Título:RNAi mediated gene silencing of ITPA using a targeted nanocarrier: Apoptosis induction in SKBR3 cancer cells.
[So] Source:Clin Exp Pharmacol Physiol;44(8):888-894, 2017 Aug.
[Is] ISSN:1440-1681
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:A pure nucleotide pool is required for high-fidelity DNA replication and prevention of carcinogenesis in living cells. Human inosine triphosphatase (ITPase), encoded by the ITPA gene, plays a critical role in maintaining the purity of the cellular nucleotide pool by excluding nucleotides that enhance mutagenesis. ITPase is a nucleoside triphosphate pyrophosphatase that hydrolyzes the non-canonical nucleotides inosine triphosphate (ITP) and xanthine triphosphate (XTP). The monophosphate products of ITPase reactions are subsequently excluded from the nucleotide pool and the improper substitution of ITP and XTP into DNA and RNA is prevented. Previous studies show that deficiency in ITPA can suppress cellular growth and enhance DNA instability. In this study, we evaluated the influence of effective ITPA down-regulation on the induction of apoptosis in a human cancer cell line using folate-single wall nanotubes (SWNT) as a targeted nanocarrier. We assessed whether SWNT enhances IPTA-siRNA transfection efficiency in cancer cells using folate as a homing device. Since folate receptor is considerably overexpressed in cancer cells, conjugation of SWNTs to folate could enhance their cancer-specific penetrance. We found that nanocarrier mediated ITPA-siRNA transfection into SKBR3 cells caused significant reduction of ITPA mRNA expression level and complete down-regulation of the ITPase protein product. The silencing of ITPA led to promotion of apoptosis in SWNT-treated SKBR3 cancer cells.
[Mh] Termos MeSH primário: Apoptose/genética
Portadores de Fármacos/química
Nanoestruturas/química
Nanotubos de Carbono/química
Pirofosfatases/deficiência
Pirofosfatases/genética
Interferência de RNA
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Regulação para Baixo/genética
Ácido Fólico/química
Seres Humanos
Hidrólise
RNA Interferente Pequeno/química
RNA Interferente Pequeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Carriers); 0 (Nanotubes, Carbon); 0 (RNA, Small Interfering); 935E97BOY8 (Folic Acid); EC 3.6.1.- (Pyrophosphatases); EC 3.6.1.19 (ITPA protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/1440-1681.12776


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[PMID]:29421518
[Au] Autor:Luo H; Liang H; Chen Y; Chen S; Xu Y; Xu L; Liu J; Zhou K; Peng J; Guo G; Lai B; Song L; Yang H; Liu L; Peng J; Liu Z; Tang L; Chen W; Tang H
[Ad] Endereço:Department of Environmental and Occupational Health, Dongguan Key Laboratory of Environmental Medicine, School of Public Health, Guangdong Medical University, Dongguan, China.
[Ti] Título:miR-7-5p overexpression suppresses cell proliferation and promotes apoptosis through inhibiting the ability of DNA damage repair of PARP-1 and BRCA1 in TK6 cells exposed to hydroquinone.
[So] Source:Chem Biol Interact;283:84-90, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Hydroquinone (HQ), one of the major metabolic products of benzene, is a carcinogen, which induces apoptosis and inhibit proliferation in lymphoma cells. microRNA-7-5p (miR-7-5p), a tumor suppressor, participates in various biological processes including cell proliferation and apoptosis regulation by repressing expression of specific oncogenic target genes. To explore whether miR-7-5p is involved in HQ-induced cell proliferation and apoptosis, we assessed the effect of miR-7-5p overexpression on induction of apoptosis analyzed by FACSCalibur flow cytometer in transfection of TK6 cells with miR-7-5p mimic (TK6- miR-7-5p). We observed an increased apoptosis by 25.43% and decreased proliferation by 28.30% in TK6-miR-7-5p cells compared to those negative control cells (TK6-shNC) in response to HQ treatment. Furthermore, HQ might active the apoptotic pathway via partly downregulation the expression of BRCA1 and PARP-1, followed by p53 activation, in TK6-miR-7-5p cells. In contrast, attenuated p53 and BRCA1 expression was observed in shPARP-1 cells than in NC cells after HQ treatment. Therefore, we conclude that HQ may activate apoptotic signals via inhibiting the tumor suppressive effects of miR-7-5p, which may be mediated partly by upregulating the expression of PARP-1 and BRCA1 in control cells. The increase of miR-7-5p expression further intensified downregulation of PARP-1 and BRCA1 in TK6-miR-7-5p cells, resulting in an increase of apoptosis and proliferation inhibited.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Proteína BRCA1/metabolismo
Proliferação Celular/efeitos dos fármacos
Reparo do DNA/efeitos dos fármacos
Hidroquinonas/farmacologia
MicroRNAs/metabolismo
Poli(ADP-Ribose) Polimerase-1/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Antagomirs/metabolismo
Proteína BRCA1/genética
Caspase 3/metabolismo
Linhagem Celular Tumoral
Regulação para Baixo/efeitos dos fármacos
Seres Humanos
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Poli(ADP-Ribose) Polimerase-1/antagonistas & inibidores
Poli(ADP-Ribose) Polimerase-1/genética
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antagomirs); 0 (BRCA1 Protein); 0 (BRCA1 protein, human); 0 (Hydroquinones); 0 (MicroRNAs); 0 (RNA, Small Interfering); 0 (Tumor Suppressor Protein p53); EC 2.4.2.30 (PARP1 protein, human); EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1); EC 3.4.22.- (Caspase 3); XV74C1N1AE (hydroquinone)
[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:180209
[St] Status:MEDLINE


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[PMID]:29336624
[Au] Autor:Zarredar H; Ansarin K; Baradaran B; Ahdi Khosroshahi S; Farajnia S
[Ad] Endereço:a Tuberculosis and Lung Disease Research Center , Tabriz University of Medical Science , Tabriz , Iran.
[Ti] Título:Potential Molecular Targets in the Treatment of Lung Cancer Using siRNA Technology.
[So] Source:Cancer Invest;36(1):37-58, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Lung cancer is the leading cause of cancer-related mortality with about 1.6 million deaths every year worldwide. Gene mutations and overexpression of oncogenes play a central role in malignant transformation in NSCLC. Conventional approaches for treatments of NSCLC have shown low levels of success while showing severe side effects. Target therapy using siRNA has recently emerged as a new strategy for cancer treatment by specific targeting of genes involved in the development and metastasis of cancer. This article dedicated to an update review of molecular targets could potentially be used for target therapy of lung cancer using SiRNA technology.
[Mh] Termos MeSH primário: Neoplasias Pulmonares/genética
RNA Interferente Pequeno/genética
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Terapia de Alvo Molecular/métodos
Mutação/genética
Metástase Neoplásica/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (RNA, Small Interfering)
[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:180117
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2017.1416393


  9 / 54562 MEDLINE  
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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


  10 / 54562 MEDLINE  
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[PMID]:28460480
[Au] Autor:Chen BJ; Zeng S; Xie R; Hu CJ; Wang SM; Wu YY; Xiao YF; Yang SM
[Ad] Endereço:Department of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, PR China.
[Ti] Título:hTERT promotes gastric intestinal metaplasia by upregulating CDX2 via NF-κB signaling pathway.
[So] Source:Oncotarget;8(16):26969-26978, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: hTERT has been reported involved in the proliferation and metastasis of gastric cancer, but the role of hTERT in gastric intestinal metaplasia, a premalignant lesion of the gastric mucosa was unknown. The aim of the present study was to investigate the role of hTERT in GIM and the effect of hTERT on CDX2 expression in gastric cells. RESULTS: Experiments showed that expression of hTERT was significantly higher in GIM than in normal gastric mucosa. Moreover, hTERT increased the KLF4 level via NF-κB during GIM. Furthermore, KLF4 is involved in the up-regulation of CDX2 induced by hTERT, and hTERT can interact with p50, thereby increasing the level of CDX2. MATERIALS AND METHODS: Immunohistochemistry was used to detect the expression of hTERT in gastric intestinal metaplasia tissue. Then, effect of hTERT on the expression of CDX2 was detected by qRT-PCR, WB and dual luciferase experiment. The role of p65 and p50 in the regulation of CDX2 were further detected by WB, CO-IP and ChIP. CONCLUSIONS: We may conclude that hTERT promotes GIM by up-regulating CDX2 via NF-κB signaling pathway.
[Mh] Termos MeSH primário: Fator de Transcrição CDX2/metabolismo
Neoplasias Gastrointestinais/genética
Neoplasias Gastrointestinais/metabolismo
NF-kappa B/metabolismo
Transdução de Sinais
Telomerase/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Fator de Transcrição CDX2/genética
Linhagem Celular Tumoral
Feminino
Neoplasias Gastrointestinais/patologia
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Fatores de Transcrição Kruppel-Like
Masculino
Metaplasia
Meia-Idade
Modelos Biológicos
Regiões Promotoras Genéticas
Ligação Proteica
RNA Interferente Pequeno/genética
Telomerase/metabolismo
Fator de Transcrição RelA/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDX2 Transcription Factor); 0 (GKLF protein); 0 (Kruppel-Like Transcription Factors); 0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (Transcription Factor RelA); EC 2.7.7.49 (TERT protein, human); EC 2.7.7.49 (Telomerase)
[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.15926



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