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Id: lil-777321
Autor: Zhou, Zhang-Yan; Zhong, Guang-Jun; Cheng, Shao-Ping; Huang, Hui; Wang, Jing; Pan, Hui; Liu, Chang-Mao; Xing, Cheng; Sun, Ya-Ling; Liu, Rong-Hua; Li, Fei.
Título: Short hairpin RNA targeting insulin-like growth factor binding protein-3 restores the bioavailability of insulin-like growth factor-1 in diabetic rats
Fonte: Int. braz. j. urol;42(1):139-145, Jan.-Feb. 2016. graf.
Idioma: en.
Projeto: National Natural Science Foundation of China.
Resumo: ABSTRACT Purpose To investigate whether intracavernosal injection of short hairpin RNA for IGFBP-3 could improve erectile function in streptozotocin-induced diabetic rats. Materials and methods After 12 weeks of IGFBP-3 short hairpin RNA injection treatment, intracavernous pressure responses to electrical stimulation of cavernous nerves were evaluated. The expression of IGFBP-3 and IGF-1 at mRNA and protein levels were detected by quantitative real-time PCR analysis and Western blot, respectively. The concentration of cavernous cyclic guanosine monophosphate was detected by enzyme-linked immunosorbent assay. Results At 12 weeks after intracavernous administration of IGFBP-3 shRNA, the cavernosal pressure was significantly increased in response to the cavernous nerves stimulation compared to the diabetic group (P<0.05). Cavernous IGFBP-3 expression at both mRNA and protein levels was significantly inhibited. At the same time, cavernous IGF-1 expression was significantly increased in the IGFBP-3 shRNA treatment group compared to the diabetic group (P<0.01). Cavernous cyclic guanosine monophosphate concentration was significantly increased in the IGFBP-3 shRNA treatment group compared to the diabetic group (P<0.01). Conclusions Gene transfer of IGFBP-3 shRNA could improve erectile function via the restoration of cavernous IGF-1 bioavailability and an increase of cavernous cGMP concentration in the pathogenesis of erectile dysfunction in streptozotocin-induced diabetic rats.
Descritores: Pênis/efeitos dos fármacos
Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/farmacocinética
RNA Interferente Pequeno/farmacocinética
Diabetes Mellitus Experimental/fisiopatologia
Disfunção Erétil/fisiopatologia
Disfunção Erétil/tratamento farmacológico
-Fator de Crescimento Insulin-Like I/análise
Fator de Crescimento Insulin-Like I/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Disponibilidade Biológica
Distribuição Aleatória
Western Blotting
Reprodutibilidade dos Testes
Ratos Wistar
Estreptozocina
Diabetes Mellitus Experimental/complicações
Reação em Cadeia da Polimerase em Tempo Real
Disfunção Erétil/etiologia
Injeções
Limites: Animais
Masculino
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


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Id: biblio-1012314
Autor: Zhang, Caixiang; Wang, Wenying; Lin, Jun; Xiao, Jing; Tian, Ye.
Título: lncRNA CCAT1 promotes bladder cancer cell proliferation, migration and invasion
Fonte: Int. braz. j. urol;45(3):549-559, May-June 2019. tab, graf.
Idioma: en.
Projeto: Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding.
Resumo: ABSTRACT Objective: To study the expression patterns of long noncoding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1) and the changes in cell proliferation, apoptosis, migration and invasion induced by silencing CCAT1 in bladder cancer cells. Materials and Methods: The expression levels of CCAT1 were determined using realtime quantitative polymerase chain reaction in cancerous tissues and paired normal tissues from 34 patients with bladder cancer. The relationship between clinical characteristics and CCAT1 expression was analyzed. And then we conducted cell experiments. Bladder urothelial carcinoma cell lines T24 and 5637 cells were transfected with CCAT1 small interfering RNA (siRNA) or scramble siRNA. Cell proliferation and apoptosis changes were determined using a Cell Counting Kit-8 (CCK-8) assay and a flow cytometry assay. Migration and invasion changes were measured using a wound healing assay and a trans-well assay. microRNAs (miRNAs) were predicted by Starbase 2.0, and their differential expression levels were studied. Results: CCAT1 was significantly upregulated in bladder cancer (P < 0.05). CCAT1 upregulation was positively related to tumor stage (P = 0.004), tumor grade (P = 0.001) and tumor size (P = 0.042). Cell proliferation, migration and invasion were promoted by abnormally expressed CCAT1. miRNAs miR-181b-5p, miR-152-3p, miR-24-3p, miR-148a-3p and miR-490-3p were potentially related to the aforementioned functions of CCAT1. Conclusion: CCAT1 plays an oncogenic role in urothelial carcinoma of the bladder. In addition, CCAT1 may be a potential therapeutic target in this cancer.
Descritores: Neoplasias da Bexiga Urinária/genética
Neoplasias da Bexiga Urinária/patologia
RNA Longo não Codificante/análise
-Sincalida/análise
Fatores de Tempo
Cicatrização/genética
Regulação para Baixo
Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Regulação para Cima
Movimento Celular/genética
MicroRNAs/genética
RNA Interferente Pequeno
Linhagem Celular Tumoral
Proliferação de Células/genética
Reação em Cadeia da Polimerase em Tempo Real
Citometria de Fluxo
Limites: Humanos
Masculino
Feminino
Idoso
Responsável: BR1.1 - BIREME


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Id: biblio-1134248
Autor: Lei, Haiming; Ma, Fujun; Jia, Renfeng; Tan, Bo.
Título: Effects of Arf6 downregulation on biological characteristics of human prostate cancer cells
Fonte: Int. braz. j. urol;46(6):950-961, Nov.-Dec. 2020. graf.
Idioma: en.
Resumo: ABSTRACT Objective To evaluate the effects of Arf6 downregulation on human prostate cancer cells. Materials and Methods The effects of Arf6 downregulation on cell proliferation, migration, invasion and apoptosis were assessed by MTT, BrdU, scratch, Transwell assays and flow cytometry respectively. AKT, p-AKT, ERK1/2, p-ERK1/2 and Rac1 protein expressions were detected by Western blot. Results Downregulating Arf6 by siRNA interference suppressed the mRNA and protein expressions of Arf6. The proliferation capacities of siRNA group at 48h, 72h, and 96h were significantly lower than those of control group (P <0.05). The migration distance of siRNA group at 18h was significantly shorter than that of control group (P <0.01). The number of cells penetrating Transwell chamber membrane significantly decreased in siRNA group compared with that of control group (P <0.01). After 24h, negative control and normal control groups had similar apoptotic rates (P >0.05) which were both significantly lower than that of siRNA group (P <0.01). After Arf6 expression was downregulated, p-ERK1/2 and Rac1 protein expressions were significantly lower than those of control group (P <0.05). Conclusion Downregulating Arf6 expression can inhibit the proliferation, migration and invasion of prostate cancer cells in vitro, which may be related to ERK1/2 phosphorylation and Rac1 downregulation.
Descritores: Neoplasias da Próstata/genética
-Regulação para Baixo
Regulação Neoplásica da Expressão Gênica
Movimento Celular
Apoptose
RNA Interferente Pequeno/genética
Linhagem Celular Tumoral
Proliferação de Células
Invasividade Neoplásica
Limites: Humanos
Masculino
Responsável: BR1.1 - BIREME


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Id: biblio-950766
Autor: Doan, Chung Chinh; Le, Long Thanh; Hoang, Son Nghia; Do, Si Minh; Van Le, Dong.
Título: Simultaneous silencing of VEGF and KSP by siRNA cocktail inhibits proliferation and induces apoptosis of hepatocellular carcinoma Hep3B cells
Fonte: Biol. Res;47:1-15, 2014. ilus, graf, tab.
Idioma: en.
Resumo: BACKGROUND: Vascular endothelial growth factor (VEGF) is involved in the growth of new blood vessels that feed tumors and kinesin spindle protein (KSP) plays a critical role in mitosis involving in cell proliferation. Simultaneous silencing of VEGF and KSP, an attractive and viable approach in cancer, leads on restricting cancer progression. The purpose of this study is to examine the therapeutic potential of dual gene targeted siRNA cocktail on human hepatocellular carcinoma Hep3B cells. RESULTS: The predesigned siRNAs could inhibit VEGF and KSP at mRNA level. siRNA cocktail showed a further downregulation on KSP mRNA and protein levels compared to KSP-siRNA or VEGF-siRNA, but not on VEGF expression. It also exhibited greater suppression on cell proliferation as well as cell migration or invasion capabilities and induction of apoptosis in Hep3B cells than single siRNA simultaneously. This could be explained by the significant downregulation of Cyclin D1, Bcl-2 and Survivin. However, no sigificant difference in the mRNA and protein levels of ANG2, involving inhibition of angiogenesis was found in HUVECs cultured with supernatant of Hep3B cells treated with siRNA cocktail, compared to that of VEGF-siRNA. CONCLUSION: Silencing of VEGF and KSP plays a key role in inhibiting cell proliferation, migration, invasion and inducing apoptosis of Hep3B cells. Simultaneous silencing of VEGF and KSP using siRNA cocktail yields promising results for eradicating hepatocellular carcinoma cells, a new direction for liver cancer treatment.
Descritores: Cinesina/genética
Apoptose/genética
Inativação Gênica
RNA Interferente Pequeno/genética
Fator A de Crescimento do Endotélio Vascular/genética
Proliferação de Células/genética
-Sais de Tetrazólio
Transfecção
Inibidores de Cisteína Proteinase/metabolismo
Regulação para Baixo
Movimento Celular
Western Blotting
Cinesina/metabolismo
Anexina A5
Genes bcl-2
Ciclina D1/metabolismo
Proteínas de Transporte Vesicular/metabolismo
Linhagem Celular Tumoral
Fator A de Crescimento do Endotélio Vascular/metabolismo
Proteínas Inibidoras de Apoptose/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Citometria de Fluxo
Survivina
Mitose/genética
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950789
Autor: Zeng, Qiangcheng; Guo, Yong; Liu, Yongming; Li, Ruixin; Zhang, Xinchang; Liu, Lu; Wang, Yang; Zhang, Xizheng; Zou, Xianqiong.
Título: Integrin-ß1, not integrin-ß5, mediates osteoblastic differentiation and ECM formation promoted by mechanical tensile strain
Fonte: Biol. Res;48:1-8, 2015. graf, tab.
Idioma: en.
Projeto: National Nature Science Foundation of China; . Science Foundation of Tianjin; . Shandong Provincial Key Laboratory of Functional Macromolecular Biophysics.
Resumo: BACKGROUND: Mechanical strain plays a great role in growth and differentiation of osteoblast. A previous study indicated that integrin-ß (ß1, ß5) mediated osteoblast proliferation promoted by mechanical tensile strain. However, the involvement of integrin-ß; in osteoblastic differentiation and extracellular matrix (ECM) formation induced by mechanical tensile strain, remains unclear. RESULTS: After transfection with integrin-ß1 siRNA or integrin-ß5 siRNA, mouse MC3T3-E1 preosteoblasts were cultured in cell culture dishes and stimulated with mechanical tensile strain of 2500 microstrain (µÎµ) at 0.5 Hz applied once a day for 1 h over 3 or 5 consecutive days. The cyclic tensile strain promoted osteoblastic differentiation of MC3T3-E1 cells. Transfection with integrin-ß1 siRNA attenuated the osteoblastic diffenentiation induced by the tensile strain. By contrast, transfection with integrin-ß5 siRNA had little effect on the osteoblastic differentiation induced by thestrain. At thesametime, theresultofECM formation promoted by the strain, was similar to the osteoblastic differentiation. CONCLUSION: Integrin-ß1 mediates osteoblast differentiation and osteoblastic ECM formation promoted by cyclic tensile strain, and integrin-ß5 is not involved in the osteoblasts response to the tensile strain.
Descritores: Osteoblastos/fisiologia
Resistência à Tração/fisiologia
Diferenciação Celular/fisiologia
Integrina beta1/fisiologia
Cadeias beta de Integrinas/fisiologia
Matriz Extracelular/fisiologia
-Estresse Mecânico
Transfecção
Linhagem Celular
Western Blotting
RNA Interferente Pequeno
Proliferação de Células/fisiologia
Reação em Cadeia da Polimerase em Tempo Real
Limites: Animais
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950812
Autor: Mikami, Taro; Yoshida, Keiichiro; Sawada, Hajime; Esaki, Michiyo; Yasumura, Kazunori; Ono, Michio.
Título: Inhibition of Rho-associated kinases disturbs the collective cell migration of stratified TE-10 cells
Fonte: Biol. Res;48:1-15, 2015. ilus, graf, tab.
Idioma: en.
Resumo: BACKGROUND: The collective cell migration of stratified epithelial cells is considered to be an important phenomenon in wound healing, development, and cancer invasion; however, little is known about the mechanisms involved. Furthermore, whereas Rho family proteins, including RhoA, play important roles in cell migration, the exact role of Rho-associated coiled coil-containing protein kinases (ROCKs) in cell migration is controversial and might be cell-type dependent. Here, we report the development of a novel modified scratch assay that was used to observe the collective cell migration of stratified TE-10 cells derived from a human esophageal cancer specimen. RESULTS: Desmosomes were found between the TE-10 cells and microvilli of the surface of the cell sheet. The leading edge of cells in the cell sheet formed a simple layer and moved forward regularly; these rows were followed by the stratified epithelium. ROCK inhibitors and ROCK small interfering RNAs (siRNAs) disturbed not only the collective migration of the leading edge of this cell sheet, but also the stratified layer in the rear. In contrast, RhoA siRNA treatment resulted in more rapid migration of the leading rows and disturbed movement of the stratified portion. CONCLUSIONS: The data presented in this study suggest that ROCKs play an important role in mediating the collective migration of TE-10 cell sheets. In addition, differences between the effects of siRNAs targeting either RhoA or ROCKs suggested that distinct mechanisms regulate the collective cell migration in the simple epithelium of the wound edge versus the stratified layer of the epithelium.
Descritores: Movimento Celular/fisiologia
RNA Interferente Pequeno/farmacologia
Quinases Associadas a rho/fisiologia
-Neoplasias Esofágicas
MicroRNAs/fisiologia
Linhagem Celular Tumoral
Quinases Associadas a rho/antagonistas & inibidores
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-973956
Autor: Pinto, Marcus Vinicius; Barreira, Amilton Antunes; Bulle, Acary Souza; Freitas, Marcos Raimundo Gomes de; França Jr, Marcondes Cavalcante; Gondim, Francisco de Assis Aquino; Marrone, Carlo Domenico; Marques Jr, Wilson; Nascimento, Osvaldo J M; Rotta, Francisco Tellechea; Pupe, Camila; Waddington-Cruz, Márcia.
Título: Brazilian consensus for diagnosis, management and treatment of transthyretin familial amyloid polyneuropathy / Consenso Brasileiro para o diagnóstico, manejo e tratamento da Polineuropatia Amiloidótica Familiar associada à Transtirretina
Fonte: Arq. neuropsiquiatr;76(9):609-621, Sept. 2018. tab, graf.
Idioma: en.
Resumo: ABSTRACT Transthyretin familial amyloid polyneuropathy is an autosomal dominant inherited sensorimotor and autonomic polyneuropathy, which if untreated, leads to death in approximately 10 years. In Brazil, liver transplant and tafamidis are the only disease-modifying treatments available. This review consists of a consensus for the diagnosis, management and treatment for transthyretin familial amyloid polyneuropathy from the Peripheral Neuropathy Scientific Department of the Brazilian Academy of Neurology. The first and last authors produced a draft summarizing the main views on the subject and emailed the text to 10 other specialists. Relevant literature on this subject was reviewed by each participant and used for the individual review of the whole text. Each participant was expected to review the text and send a feedback review by e-mail. Thereafter, the 12 panelists got together at the city of Fortaleza, discussed the controversial points, and reached a consensus for the final text.

RESUMO Polineuropatia amiloidótica familiar é uma polineuropatia sensitivo-motora e autonômica de herança autossômica dominante, que caso não seja tratada leva a morte em aproximadamente 10 anos. O transplante de fígado e o tafamidis são os únicos tratamentos disponíveis no Brasil. Essa revisão consiste em um consenso do Departamento Científico de Neuropatias Periféricas da Academia Brasileira de Neurologia. O primeiro e último autores produziram um texto resumindo os principais aspectos sobre o tema e enviaram para os outros 10 especialistas por email. A literatura relevante sobre o assunto foi revisada por cada participante e utilizada para revisão individual do texto. Foi esperado que cada participante revisasse o texto e enviasse suas sugestões por e-mail. Finalmente, os 12 panelistas se encontraram na cidade de Fortaleza para discutir os pontos controversos e chegar a um consenso sobre texto final.
Descritores: Neuropatias Amiloides Familiares/diagnóstico
Neuropatias Amiloides Familiares/terapia
-Oligonucleotídeos/uso terapêutico
Benzoxazóis/uso terapêutico
Brasil
Ensaios Clínicos Controlados Aleatórios como Assunto
Neuropatias Amiloides Familiares/patologia
Neuropatias Amiloides Familiares/tratamento farmacológico
RNA Interferente Pequeno/uso terapêutico
Diagnóstico Diferencial
Cardiomiopatias/complicações
Limites: Humanos
Animais
Tipo de Publ: Conferência de Consenso
Responsável: BR1.1 - BIREME


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Id: biblio-1041054
Autor: Huang, Yayi; Zhou, Fang; Xiao, Yeda; Shen, Cheng; Liu, Kang; Zhao, Bo.
Título: TLR7 mediates increased vulnerability to ischemic acute kidney injury in diabetes
Fonte: Rev. Assoc. Med. Bras. (1992);65(8):1067-1073, Aug. 2019. graf.
Idioma: en.
Projeto: Hubei Province.
Resumo: SUMMARY OBJECTIVE Diabetes is a risk factor for acute kidney injury (AKI). However, its mechanism of pathogenesis has not been elucidated. The aim of the study was to investigate the role of inflammation and the toll-like receptor 7 (TLR7) in ischemic AKI for diabetes. METHODS A high glucose hypoxia-reoxygenation model of human renal tubular epithelial (HK-2) cells was used to generate AKI induced by ischemia-reperfusion in diabetes. The activity of cells was measured by CCK-8 assay and LDH activity. Inflammatory cytokines were assessed by ELISA. TLR7, MyD88, and NF-κB expressions were examined by western blotting. Apoptosis was evaluated by flow cytometry. RESULTS The high glucose group and low glucose group were subjected to hypoxia-reoxygenation. The low glucose group developed only mild cell damage, apoptosis, and inflammatory response. In contrast, an equivalent hypoxia-reoxygenation injury provoked severe cell damage, apoptosis, and inflammatory response in the high glucose group. Expression of TLR7 and its related proteins were measured in the high glucose group before and after hypoxia-reoxygenation. The high glucose group exhibited more significant increases in TLR7 expression following hypoxia-reoxygenation than the low glucose group. In addition, the expression of TLR7 and its related proteins after hypoxia-reoxygenation were higher in the high glucose group than in the low glucose group. Inhibition of TLR7 provides significant protection against ischemic injury in diabetes. CONCLUSION Our results suggest that diabetes increases the vulnerability to ischemia-induced renal injury. This increased vulnerability originates from a heightened inflammatory response involving the TLR7 signal transduction pathway.

RESUMO OBJETIVO O diabetes é um fator de risco para a lesão renal aguda (LRA). No entanto, seu mecanismo de patogênese não foi elucidado. O objetivo do estudo foi investigar o papel da inflamação e do receptor Toll-like 7 (TLR7) na LRA isquêmica no diabetes. MÉTODOS Um modelo de hipóxia-reoxigenação de células epiteliais tubulares renais humanas (HK-2) na presença de concentrações altas de glicose foi utilizado para gerar LRA induzida por isquemia-reperfusão em diabetes. A atividade das células foi medida pelo ensaio Cell Counting Kit-8 (CCK-8) e pela atividade da lactato desidrogenase (LDH). As citocinas inflamatórias foram avaliadas por ensaio imunoenzimático (Elisa). A expressão de TLR7, do fator de diferenciação mieloide 88 (MyD88) e do fator de transcrição nuclear-κB (NF-κB) foi examinada por Western blotting. A apoptose foi avaliada por citometria de fluxo. RESULTADOS Os grupos glicose alta e glicose baixa foram submetidos à hipóxia-reoxigenação. O grupo de baixa glicose desenvolveu apenas danos celulares ligeiros, apoptose e uma resposta inflamatória. Em contraste, no grupo de alta glicose, uma lesão equivalente de hipóxia-reoxigenação provocou danos celulares graves, apoptose e uma resposta inflamatória. A expressão de TLR7 e suas proteínas relacionadas foi medida no grupo de alta glicose antes e após a hipóxia-reoxigenação. O grupo de alta glicose exibiu maiores aumentos na expressão de TLR7 após hipóxia-reoxigenação do que o grupo de baixa glicose. Além disso, a expressão de TLR7 e suas proteínas relacionadas após a hipóxia-reoxigenação foi maior no grupo com alto nível de glicose do que no grupo com baixo nível de glicose. A inibição do TLR7 fornece proteção significativa contra a lesão isquêmica no diabetes. CONCLUSÃO Nossos resultados sugerem que o diabetes aumenta a vulnerabilidade à lesão renal induzida por isquemia. Essa vulnerabilidade acrescida tem por origem uma resposta inflamatória aumentada envolvendo a via de transdução de sinal do TLR7.
Descritores: Diabetes Mellitus/metabolismo
Receptor 7 Toll-Like/metabolismo
Injúria Renal Aguda/metabolismo
Isquemia/metabolismo
-Transfecção
Transdução de Sinais
Células Cultivadas
RNA Interferente Pequeno
Diabetes Mellitus/fisiopatologia
Receptor 7 Toll-Like/fisiologia
Injúria Renal Aguda/fisiopatologia
Citometria de Fluxo
Isquemia/fisiopatologia
Limites: Humanos
Responsável: BR1.1 - BIREME


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Id: biblio-1055510
Autor: Chen, Jing; Li, Hai Liang; Li, Bo Bo; Li, Wei; Ma, Dong; Li, Yong He; Liu, Tao.
Título: Serum- and glucocorticoid-inducible kinase 3 is a potential oncogene in nasopharyngeal carcinoma / Quinase 3 sérica induzida por glicocorticoide é um potencial oncogene no carcinoma nasofaríngeo
Fonte: Braz. j. otorhinolaryngol. (Impr.);85(6):705-715, Nov.-Dec. 2019. tab, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China.
Resumo: Abstract Introduction: Serum- and glucocorticoid-inducible kinase 3, a serine/threonine kinase that functions downstream of the PI3K signaling pathway, plays a critical role in neoplastic processes. It is expressed by various tumors and contributes to carcinogenesis. Objective: The objective was to investigate serum- and glucocorticoid-inducible kinase 3 expression in nasopharyngeal carcinoma, to study the anti-tumor effects of serum- and glucocorticoid-inducible kinase 3 shRNA by inhibiting its expression in nasopharyngeal carcinoma cells and to discuss the potential implications of our findings. Methods: Serum- and glucocorticoid-inducible kinase 3 protein expression in nasopharyngeal carcinoma cell lines (CNE-1, CNE-2, HNE-1, HONE-1, and SUNE-1) and the human immortalized nasopharyngeal epithelium cell line NP69 were assayed by western blotting. Serum- and glucocorticoid-inducible kinase 3 expression in 42 paraffin-embedded nasopharyngeal carcinoma tissues were performed by immunohistochemistry. MTT assay, flow cytometry, and scratch tests were performed after CNE-2 cells were transfected with the best serum- and glucocorticoid-inducible kinase 3 shRNA plasmid selected by western blotting using lipofectamine to study its effect on cell proliferation, apoptosis, and migration. Results: Serum- and glucocorticoid-inducible kinase 3 was overexpressed in human nasopharyngeal carcinoma tissues and cells. Serum- and glucocorticoid-inducible kinase 3 expression decreased markedly after CNE-2 cells were transfected with the serum- and glucocorticoid-inducible kinase 3 shRNA, leading to strong inhibition of cell proliferation and migration. In addition, the apoptosis rate increased in CNE-2 cells after serum- and glucocorticoid-inducible kinase 3 knockdown. Conclusion: Serum- and glucocorticoid-inducible kinase 3 expression was more frequently observed as the nasopharyngeal epithelium progresses from normal tissue to carcinoma. This suggests that serum- and glucocorticoid-inducible kinase 3 contributes to the multistep process of NPC carcinogenesis. Serum- and glucocorticoid-inducible kinase 3 represents a target for nasopharyngeal carcinoma therapy, and a basis exists for the further investigation of this adjuvant treatment modality for nasopharyngeal carcinoma.

Resumo Introdução: A quinase 3 sérica induzida por glicocorticoide, uma serina/treonina quinase que funciona downstream da via de sinalização PI3K, desempenha um papel crítico nos processos neoplásicos. É expressa por vários tumores e contribui para a carcinogênese. Objetivo: Investigar a expressão de quinase 3 sérica induzida por glicocorticoide no carcinoma nasofaríngeo, estudar os efeitos antitumorais do shRNA da quinase 3 sérica induzida por glicocorticoide, que inibem sua expressão em células de carcinoma nasofaríngeo, e discutir as implicações potenciais de nossos achados. Método: A expressão de proteína quinase 3 sérica induzida por glicocorticoide em linhagens de células de carcinoma nasofaríngeo (CNE-1, CNE-2, HNE-1, HONE-1 e SUNE-1) e a linhagem de células humanas imortalizadas do epitélio nasofaríngeo NP69 foram avaliadas por Western blot. A expressão da quinase 3 sérica induzida por glicocorticoide em 42 tecidos de CNF embebidos em parafina foi feita por imuno-histoquímica. Testes com MTT, citometria de fluxo e testes de raspagem foram feitos após as células CNE-2 terem sido transfectadas com o melhor plasmídeo shRNA da quinase 3 sérica induzida por glicocorticoide selecionado por Western blot, com o uso de lipofectamina para estudar seu efeito na proliferação, apoptose e migração celular. Resultados: Foi observada uma sobre-expressão da quinase 3 sérica induzida por glicocorticoide em tecidos e células de carcinoma nasofaríngeo humanas. A expressão de quinase 3 sérica induzida por glicocorticoide diminuiu acentuadamente após as células CNE-2 terem sido transfectadas com o shRNA da quinase 3 sérica induzida por glicocorticoide, conduzindo a forte inibição de proliferação e migração celular. Além disso, a taxa de apoptose aumentou nas células CNE-2 após o knockdown da quinase 3 sérica induzida por glicocorticoide. Conclusão: A expressão de quinase 3 sérica induzida por glicocorticoide foi observada com maior frequência à medida que o epitélio nasofaríngeo progride de tecido normal para carcinoma. Isso sugere que a quinase 3 sérica induzida por glicocorticoide contribui para o processo multietapas da carcinogênese do carcinoma nasofaríngeo. A quinase 3 sérica induzida por glicocorticoide representa um alvo para a terapia do carcinoma nasofaríngeo e há uma base para a investigação adicional dessa modalidade de tratamento adjuvante para o carcinoma nasofaríngeo.
Descritores: Neoplasias Nasofaríngeas/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Imediatamente Precoces/metabolismo
Carcinoma Nasofaríngeo/metabolismo
-Imuno-Histoquímica
Movimento Celular/efeitos dos fármacos
Neoplasias Nasofaríngeas/patologia
Nasofaringite/metabolismo
Nasofaringite/patologia
Proteínas Serina-Treonina Quinases/farmacologia
Apoptose
Proteínas Imediatamente Precoces/farmacologia
RNA Interferente Pequeno/metabolismo
Proliferação de Células/efeitos dos fármacos
Carcinoma Nasofaríngeo/patologia
Limites: Humanos
Masculino
Feminino
Adulto
Pessoa de Meia-Idade
Responsável: BR1.1 - BIREME


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Id: biblio-1139172
Autor: Cuello Almarales, Dany A; Almaguer Mederos, Luis E; Almaguer Gotay, Dennis.
Título: Potencial uso terapéutico del ARN de interferencia contra la COVID-19 / Potential therapeutic use of RNA interference against COVID-19
Fonte: Rev. habanera cienc. méd;19(4):e3400graf.
Idioma: es.
Resumo: Introducción: El SARS-CoV-2 es el agente causal de la COVID-19, enfermedad respiratoria que ha causado miles de víctimas fatales a escala global, y para la cual no existe ninguna terapia curativa efectiva. Objetivo: Reflejar la relevancia potencial de la tecnología de ARN de interferencia (ARNi), como alternativa terapéutica contra la COVID-19. Material y métodos: Se consultaron las bases de datos especializadas en busca de artículos publicados hasta abril de 2020. Se emplearon descriptores específicos y operadores booleanos. Se empleó la estrategia de búsqueda avanzada para la selección de los artículos, teniendo en cuenta la calidad metodológica o validez de los estudios. Desarrollo: Fueron identificadas evidencias de aplicación a nivel experimental de la tecnología de ARNi contra el SARS-CoV. Se han diseñado y evaluado varios ARNs pequeños interferentes y ARNs pequeños con estructura en lazo, orientados al silenciamiento de genes esenciales del SARS-CoV, incluyendo aquellos que codifican las proteínas S, RdRp, M, E, N, 3a/3b y 7a/7b. Se comprobó la efectividad de los ARNi en el silenciamiento de sus genes diana. Aunque la mayoría de estas investigaciones se han realizado en sistemas in vitro, también se ha comprobado la utilidad terapéutica de la administración intranasal de ARNi en un modelo de SARS-CoV in vivo. Conclusiones: La tecnología de ARNi ha mostrado potencialidades como estrategia terapéutica contra el SARS-CoV en modelos celulares y animales. Dadas las similitudes a nivel genómico y en cuanto al proceso patogénico entre SARS-CoV y SARS-CoV-2, esta tecnología es potencialmente aplicable el tratamiento de la COVID-19(AU)

Introduction: SARS-CoV-2 is the causal agent of COVID-19, a respiratory disease that has caused thousands of deaths globally for which there is no effective curative therapy. Objective: To demonstrate the potential relevance of RNA interference (RNAi) technology as a therapeutic alternative in the treatment of COVID-19. Materials and methods: Specialized biomedical databases were searched looking for studies published until April 2020. The search was carried out using descriptors and Boolean operators. Advanced search strategy was used for the selection of articles, taking into account the methodological quality and validity of the studies. Results: Evidence of experimental application of RNAi technology against SARS-CoV was identified. Several small interfering RNAs and small loop-structured RNAs oriented to the silencing of essential SARS-CoV genes including those encoding the S, RdRp, M, E, N, 3a/3b and 7a/7b proteins have been designed and evaluated. The effectiveness of RNAi for silencing its target genes was proven. Although most of these research studies have been conducted in in vitro systems, the therapeutic effectiveness of the intranasal administration of small RNA interference has also been proven in an in vivo SARS-CoV model. Conclusions: RNAi technology has demonstrated to be a potential therapeutic strategy against SARS-CoV in cellular and animal models. Given the similarities at the genomic level and in terms of the pathogenic process between SARS-CoV and SARS-CoV-2, this technology has a potential applicability for the treatment of COVID-19(AU)
Descritores: Infecções por Coronavirus/terapia
RNA Interferente Pequeno/uso terapêutico
Responsável: CU1.1 - Biblioteca Médica Nacional



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