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  1 / 19 LILACS  
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Id: biblio-1089072
Autor: Zhao, Jun; Geng, Lijiao; Chen, Yong; Wu, Chunfang.
Título: SNHG1 promotes MPP+-induced cytotoxicity by regulating PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells via sponging miR-153-3p
Fonte: Biol. Res;53:01, 2020. graf.
Idioma: en.
Resumo: BACKGROUND: Long non-coding RNA small molecule RNA host gene 1 (SNHG1) was previously identified to be relevant with Parkinson's disease (PD) pathogenesis. This work aims to further elucidate the regulatory networks of SNHG1 involved in PD. Methods: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-hydrochloride (MPTP)-induced mice and 1-methyl-4-phenylpyridinium (MPP+)-treated SH-SY5Y cells were respectively constructed as the in vivo and in vitro PD models. Expression levels of SNHG1 and miR-153-3p were detected by qRT-PCR. Protein expression levels of phosphate and tension homology deleted on chromosome ten (PTEN) were measured by western blotting assay. Cell viability and apoptosis were determined by MTT and flow cytometry assays. The interactions among SNHG1, miR-153-3p and PTEN were identified by luciferase reporter assay, RNA immunoprecipitation, and/or RNA pull-down analysis. RESULTS: Increased SNHG1 expression was found in midbrain of MPTP-induced PD mice and MPP+-treated SH-SY5Y cells. Overexpression of SNHG1 lowered viability and enhanced apoptosis in MPP+-treated SH-SY5Y cells. Moreover, SNHG1 acted as a molecular sponge to inhibit the expression of miR-153-3p. Furthermore, miR-153-3p-mediated suppression of MPP+-induced cytotoxicity was abated following SNHG1 up-regulation. Additionally, PTEN was identified as a direct target of miR-153-3p, and SNHG1 could serve as a competing endogenous RNA (ceRNA) of miR-153-3p to improve the expression of PTEN. Besides, enforced expression of PTEN displayed the similar functions as SNHG1 overexpression in regulating the viability and apoptosis of MPP+-treated SH-SY5Y cells. Finally, SNHG1 was found to activate PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells by targeting miR-153-3p. CONCLUSION: SNHG1 aggravates MPP+-induced cellular toxicity in SH-SY5Y cells by regulating PTEN/AKT/mTOR signaling via sponging miR-153-3p, indicating the potential of SNHG1 as a promising therapeutic target for PD.
Descritores: Doença de Parkinson/metabolismo
1-Metil-4-fenilpiridínio/toxicidade
PTEN Fosfo-Hidrolase/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Serina-Treonina Quinases TOR/metabolismo
RNA Longo não Codificante/metabolismo
-Doença de Parkinson/genética
Transfecção
Transdução de Sinais
Células Cultivadas
Regulação da Expressão Gênica
Western Blotting
Apoptose
MicroRNAs
Modelos Animais de Doenças
Reação em Cadeia da Polimerase em Tempo Real
RNA Longo não Codificante/genética
Camundongos Endogâmicos C57BL
Limites: Animais
Masculino
Camundongos
Responsável: CL1.1 - Biblioteca Central


  2 / 19 LILACS  
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Id: biblio-870247
Autor: Schultz, Luciana.
Título: Valor prognóstico de phosS6 e modulação da via mTOR em produtos decistectomia / phosS6 prognostic value and mTOR pathway modulation in cystectomy specimens.
Fonte: São Paulo; s.n; 2015. 102 p. ilust, tabelas, quadros.
Idioma: pt.
Tese: Apresentada a Fundação Antônio Prudente para obtenção do grau de Doutor.
Resumo: Introdução: O carcinoma urotelial da bexiga é uma doença de alta incidência e letalidade. Em tumores avançados, há indicação de quimioterapia com agentes convencionais, porém a sobrevida global em 5 anos não excede 15%. A via mTOR é essencial para vários processos celulares, incluindo metabolismo, proliferação, angiogênese e diferenciação celular, e, estando alterada em mais de 40% dos tumores uroteliais, representa uma opção atraente para inibição farmacológica. No entanto, até o momento, os ensaios clínicos não têm desempenhado de forma satisfatória, o que se atribui à falta de critérios robustos para definição terapêutica e a particularidades de sua patogênese, as quais incluem retroalimentações da própria via, desta com outras vias essenciais e regulações pós-transcricionais críticas. Metodologia: Analisamos a expressão proteica (imunoistoquímica, n=101) e gênica (RT-PCR, n=78) de diversos componentes da via mTOR e de suas principais vias interativas (via induzida por hipóxia e ciclo celular), assim como o perfil de expressão de miRNAs (n=72), em amostras neoplásicas e não-neoplásicas obtidas de pacientes submetidos a cistectomia. A expressão proteica e gênica dos tumores foi quantificada em relação às de amostras não-neoplásicas, enquanto a interação entre genes e entre proteínas foi avaliada através de análise dendrológica. Para a análise das relações entre expressão proteica e gênica, a expressão proteica foi categorizada por meio de análise por cluster seguida de curva ROC e a expressão gênica foi transformada em escore através de lógica fuzzy. Os valores de expressão de miRNAs foram comparados por teste t, partindo das categorias criadas para phosS6 (Ser 235/236), seguido-se de análise por cluster...

Introduction: Urothelial carcinoma of the bladder is highly incident and lethal. In advanced disease, conventional chemotherapy may be applied, but overall 5-year survival does not exceed 15%. The mTOR pathway is essential to many cellular processes, including metabolism, proliferation, angiogenesis and cell differentiation and, since it is altered in > 40% of urothelial tumors, it represents an attractive target for pharmacological inhibition. However, clinical trials have not yielded exciting results, which is attributed to the lack of robust criteria for therapeutic definition and particularities of its pathogenesis, represented by feedback mechanisms along the pathway itself and with other essential pathways, as well as critical posttranscriptional regulation steps. Methods: Protein and gene expression of mTOR pathway members and its interacting pathway components (hypoxia-inducible pathway and cell cycle) were analyzed by IHC (n=101), RT-PCR (n=78) and miRNA profiling (n=72), in neoplastic and non-neoplastic samples obtained from patients submitted to cystectomy. Gene and protein expression were quantified relatively to non-neoplastic urothelial tissue and interaction between the genes and between the proteins was analyzed using dendrograms...
Descritores: Carcinoma
Expressão Gênica
Imuno-Histoquímica
MicroRNAs/genética
Neoplasias da Bexiga Urinária
Prognóstico
-Serina-Treonina Quinases TOR
Limites: Humanos
Responsável: BR30.1 - Biblioteca
BR30.1


  3 / 19 LILACS  
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Id: biblio-1051305
Autor: Wang, Heyuan; Wu, Bing; Wang, Haotian.
Título: Alpha-hederin induces the apoptosis of oral cancer SCC-25 cells by regulating PI3K/Akt/mTOR signaling pathway
Fonte: Electron. j. biotechnol;38:27-31, Mar. 2019. graf, ilus.
Idioma: en.
Projeto: Jilin Provincial Industrial Innovation Special Fund Project; . Jilin Province Chinese Medicine Science and Technology.
Resumo: BACKGROUND: Oral cancer is one of the common malignant tumors of the head and neck. However, current treatments have numerous side effects, and drugs from natural sources may have better therapeutic potential. This research investigated the induction of apoptosis by α-hederin (α-HN), a constituent of Pulsatilla chinensis (Bunge) Regel, in the oral cancer cell line SCC-25 and its underlying mechanism. RESULTS: SCC-25 cells were treated with 50, 100, and 200 µmol/L α-HN. Cell proliferation; extent of apoptosis; activities of caspases-3, 8, and 9; and the expression of Bcl-2, Bax, phosphorylated (p)-phosphoinositide 3-kinase (PI3K), p-Akt, and p-mammalian target of rapamycin (mTOR) proteins were determined using the 3-(4,5)-2-thiazole-(2,5)-diphenyl tetrazolium bromide, flow cytometry, caspase activity detection kits, and western blot assays, respectively. The results showed that the proliferation of SCC-25 cells in the α-HN-treated groups decreased significantly, and the inhibitory effect was time and concentration dependent. Compared with cells in the control group, the extent of apoptosis increased significantly, caspase-3 and -9 activities were significantly enhanced, and the Bcl-2 level was lowered and the Bax level was elevated significantly in SCC-25 cells treated with α-HN for 48 h (P b 0.05). The expression of p-PI3K, p-Akt, and p-mTOR was also significantly lower in SCC-25 cells treated with α-HN than that in the control group (P b 0.05). CONCLUSION: These results indicate that α-HN can inhibit proliferation and induce apoptosis of SCC-25 cells and may exert these effects by inhibiting the PI3K/Akt/mTOR signaling pathway.
Descritores: Ácido Oleanólico/análogos & derivados
Saponinas/farmacologia
Neoplasias Bucais/metabolismo
Apoptose/efeitos dos fármacos
-Ácido Oleanólico/metabolismo
Ácido Oleanólico/farmacologia
Saponinas/metabolismo
Transdução de Sinais/efeitos dos fármacos
Sobrevivência Celular
Western Blotting
Fosfatidilinositol 3-Quinases/metabolismo
Caspases
Pulsatilla
Proliferação de Células/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Serina-Treonina Quinases TOR/metabolismo
Citometria de Fluxo
Neoplasias de Cabeça e Pescoço/metabolismo
Responsável: CL1.1 - Biblioteca Central


  4 / 19 LILACS  
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Id: lil-756692
Autor: Rodrigues, Iara Sant'Ana.
Título: Avaliação do processo de transição epitélio-mesênquima e sua correlação com tipos virais de HPV e terapia em carcinomas vulvares / Evaluation of the epithelial mesenchymal transition process and its correlation with viral HPV types and terapy in vulvar carcinomas.
Fonte: São Paulo; s.n; 2014. 146 p. ilus, tab, quadros.
Idioma: pt.
Tese: Apresentada a Fundação Antônio Prudente para obtenção do grau de Doutor.
Resumo: O carcinoma de células escamosas da vulva compreende 92% de todos os tipos de câncer vulvar invasivo e corresponde a cerca de 3% a 5% dos tumores malignos do trato genital feminino. A transição epitelio mesênquima (TEM) é um importante evento durante a progressão do câncer e é induzida via ativação de fatores de transcrição como TWIST, SNAI2 e SNAI1 que modulam a expressão de E-caderina, Vinentina e β-catenina. Entretanto, para o carcinoma vulvar pouco se sabe sobre a relação da TEM com a presença de tipos específicos de papiloma vírus humano (HPV), fatores prognósticos e terapia. Mediante tal contexto, os objetivos do presente estudo foram identificar as alterações de expressão proteica de marcadores de transição epitélio-mesênquima (TEM) comparando centro e fronte do tumor e correlacionar os resultados com a presença de infecção por subtipos específicos de HPV para a determinação de valores prognósticos e preditivos em carcinoma de vulva. Também realizamos ensaios in vitro para observar o efeito de NVP-BEZ235, um composto que age indiretamente em fatores de transcrição como o Slug, em uma linhagem metastática de vulva. Nossos resultados demonstraram que a perda de expressão de E-caderina é observada em estágios avançados de invasão tumoral enquanto que β-catenina representa um biomarcador importante para estabelecer o prognóstico no carcinoma vulvar (p=0.044). Além disso, a perda de expressão de β-catenina associada ao aumento de expressão de Slug no fronte de invasão caracteriza um subgrupo de tumores com fenótipo de TEM relacionados com a negatividade para infecção pelo HPV com o pior prognóstico (p = 0,001). No cenário clínico, a avaliação de imuno-histoquímica comparativa da expressão de β-catenina entre fronte de invasão e centro do tumor, pode representar uma ferramenta adicional para estabelecer o prognóstico de carcinoma vulvar...

Vulvar squamous cell carcinoma comprises 92% of all cases of vulvar cancer and accounts for about 3% to 5% of malignant tumors of the female genital tract. Epithelial-mesenchymal transition (EMT) is an important event during cancer progression and it is induced by activation of transcription factors as Twist, Slug and Snail factors that modulate the expression of E-cadherin, Vimentin and B-catenin. However, considering vulvar carcinoma, little is known about the relationship among EMT, presence of specific types of human papillomavirus (HPV), prognostic factors and therapy. In this context, the aims of this study were to analyze expression of markers of EMT comparing invasive front and central tumor and correlate the results with the presence of specific subtypes of HPV for determination of prognostic and predictive factors in vulvar carcinoma. And also we performed in vitro assays to observe the effect of NVP-BEZ235, a compound that acts indirectly on transcription factors such as Slug on a metastatic vulvar cancer cell line. Our results demonstrated that loss of E-cadherin expression is observed in advanced stages of tumor invasion whereas β-catenin is an important biomarker for establishing the prognosis in vulvar carcinoma (p=0.044). Furthermore, β-catenin lower expression associated with gain in Slug expression at the invasive front characterizes a subgroup of EMT-related HPV-negative tumors with the worst outcome, increased invasiveness and progression (p= 0.001). In the clinical setting, IHC comparative assessmentof β-catenin expression between invasive front and central tumor may represent an additional tool for establishing prognosis of vulvar cancer. We also showed that NVP-BEZ235 decreased the migration, invasion and proliferation of metastatic vulvar cancer cell line that presents an EMT-like that represents a potential therapeutic target for the treatment of aggressive tumors, which often do not respond to conventional treatments...
Descritores: Infecções por Papillomavirus
Neoplasias Vulvares/diagnóstico
Serina-Treonina Quinases TOR
Transição Epitelial-Mesenquimal
Limites: Humanos
Responsável: BR30.1 - Biblioteca
BR30.1


  5 / 19 LILACS  
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Id: biblio-1011404
Autor: Li, Ling; Liu, Ming; Zhang, Zhihu; Zhang, Wei; Liu, Naifu; Sheng, Xiugui; Wei, Ping.
Título: Derlin1 functions as an oncogene in cervical cancer via AKT/mTOR signaling pathway
Fonte: Biol. Res;52:8, 2019. tab, graf.
Idioma: en.
Resumo: BACKGROUND: Cervical cancer (CC) ranks third in the morbidity and mortality of female cancer around the world. Derlin1 has been found to be overexpressed in several human cancers. However, it is still unclear about its roles in CC. The research aims to explore the relationship between Derlin1 and CC. METHODS: We purchased a human CC tissues microarray, which contained CC tissues and corresponding para-cancerous tissues from 93 patients with primary cervical squamous cell carcinoma. Immunohistochemical staining was used to confirm the expression of Derlin1 in these tissues. And we detected the differential expression of Derlin1 in cervical cancer cell lines and normal cervical epithelial cells (H8). Further, the cervical cancer cell lines SiHa and C33A were used as an in vitro model, which was down-regulated the expression of Derlin1 using siRNA interference technology. The effects of Derlin1 down-regulating in CC cell lines on cell proliferation and migration were detected by CCK8 assay and transwell assay, respectively. The effect of Derlin1 down-regulating on apoptosis was analyzed by flow cytometry, and apoptosis-related proteins were detected using western blotting. In-depth mechanisms were studied using western blotting. In addition, the effects of Derlin1 up-regulating in normal cervical epithelial cells also were exposed. RESULTS: Derlin1 was significantly elevated in CC tissues (81.7%, 76/93), and the expression of Derlin 1 was positively correlated with the tumor size, pathological grade, and lymph node metastasis in CC patients. And Derlin 1 was high expressed in cervical cancer cell lines compared to H8 cells. Knockdown of Derlin 1 in cervical cancer cell lines inhibited cell proliferation and migration. Moreover, knockdown of Derlin 1 induced apoptosis and affected the expression of apoptosis-related proteins, including Bcl-2, Bax, Bim, caspase3 and caspase9. Further experiments showed that AKT/mTOR signal pathway might be involve in this processes that knockdown of Derlin 1 inhibited the expression of p-AKT and p-mTOR. Over-expression of Derlin 1 in H8 cells promoted cell proliferation and migration via up-regulated the expression of p-AKT and p-mTOR. CONCLUSION: Derlin 1 is an oncogene in CC via AKT/mTOR pathway. It might be a potential therapeutic target for CC.
Descritores: Carcinoma de Células Escamosas/metabolismo
Transdução de Sinais/fisiologia
Neoplasias do Colo do Útero/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Serina-Treonina Quinases TOR/metabolismo
Proteínas de Membrana/metabolismo
-Imuno-Histoquímica
Carcinoma de Células Escamosas/patologia
Neoplasias do Colo do Útero/patologia
Apoptose
Análise Serial de Proteínas
Linhagem Celular Tumoral
Proliferação de Células
Proteínas Proto-Oncogênicas c-akt/fisiologia
Limites: Humanos
Feminino
Tipo de Publ: Carta
Responsável: CL1.1 - Biblioteca Central


  6 / 19 LILACS  
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Id: biblio-1011410
Autor: Liu, Xiaoli; Jiang, Qingfeng; Liu, Huaimin; Luo, Suxia.
Título: Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells
Fonte: Biol. Res;52:7, 2019. graf.
Idioma: en.
Resumo: BACKGROUND: Currently, the prognosis of patients with non-small cell lung cancer (NSCLC) remains dismal; hence, it is critical to identify effective anti-NSCLC agents with limited side effects. This study aimed to evaluate the therapeutic potential of flavonoid compound vitexin in human NSCLC cells and the underlying mechanisms. RESULTS: The experimental results indicated that vitexin reduced the viability of A549 cells in a dose-dependent manner with nearly no toxicity against normal human bronchial epithelial 16HBE cells. Vitexin also dose-dependently increased A549 cell apoptosis, accompanied by the decreased Bcl-2/Bax ratio and the increased expression of cleaved caspase-3. Moreover, the in vivo anticancer activity of vitexin was further determined in nude mice bearing A549 cells. In addition, vitexin induced the release of cytochrome c from the mitochondria to the cytosol and the loss of mitochondrial membrane potential. Vitexin also significantly reduced the levels of p-PI3K, p-Akt and p-mTOR, and the pro-apoptotic effect of vitexin on A549 cells was partly blocked by SC79, an Akt activator. CONCLUSIONS: Accordingly, we believed that vitexin could be used as a potential therapeutic agent for the treatment of NSCLC in the future.
Descritores: Apoptose/efeitos dos fármacos
Carcinoma Pulmonar de Células não Pequenas/patologia
Fosfatidilinositol 3-Quinases/efeitos dos fármacos
Apigenina/farmacologia
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Serina-Treonina Quinases TOR/efeitos dos fármacos
Neoplasias Pulmonares/patologia
Antineoplásicos/farmacologia
-Transdução de Sinais/efeitos dos fármacos
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Linhagem Celular Tumoral
Proliferação de Células/efeitos dos fármacos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Células A549
Neoplasias Pulmonares/metabolismo
Camundongos Nus
Mitocôndrias/efeitos dos fármacos
Limites: Humanos
Animais
Camundongos
Responsável: CL1.1 - Biblioteca Central


  7 / 19 LILACS  
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Id: biblio-1014279
Autor: Arancibia, Javiera; Labbé, Tomas P; Ríos, Juvenal A.
Título: mTOR, autofagia y cáncer: ad portas del nuevo decreto de la Ley Ricarte Soto / mTOR inhibitors, autophagia and Cancer: looking forward to a universal financial coverage
Fonte: Rev. méd. Chile;147(5):674-676, mayo 2019.
Idioma: es.
Descritores: Autofagia/fisiologia
Serina-Treonina Quinases TOR/antagonistas & inibidores
Serina-Treonina Quinases TOR/metabolismo
Neoplasias/tratamento farmacológico
Antineoplásicos/uso terapêutico
-Sirolimo/análogos & derivados
Sirolimo/economia
Sirolimo/uso terapêutico
Everolimo/economia
Everolimo/uso terapêutico
Neoplasias/metabolismo
Antineoplásicos/economia
Limites: Humanos
Tipo de Publ: Carta
Responsável: CL1.1 - Biblioteca Central


  8 / 19 LILACS  
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Id: biblio-1100910
Autor: Hu, Hao; Wu, Jiawei; Yu, Xiaofan; Zhou, Junling; Yu, Hua; Ma, Likun.
Título: Long non-coding RNA MALAT1 enhances the apoptosis of cardiomyocytes through autophagy inhibition by regulating TSC2-mTOR signaling
Fonte: Biol. Res;52:58, 2019. graf.
Idioma: en.
Projeto: National Natural Science Foundation of China.
Resumo: BACKGROUND: Our previous study showed that knockdown of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) attenuated myocardial apoptosis in mouse acute myocardial infarction (AMI). This study aims to explore whether MALAT1 enhanced cardiomyocyte apoptosis via autophagy regulation and the underlying mechanisms of MALAT1 regulating autophagy. METHODS: Cardiomyocytes were isolated from neonatal mice and then stimulated with hypoxia/reoxygenation (H/R) injury to mimic AMI. The autophagy level was assessed using GFP-LC3 immunofluorescence and western blot analysis of autophagy-related proteins. RNA pull-down and RNA immunoprecipitation (RIP) was performed to analyze the binding of MALAT1 and EZH2. Chromatin immunoprecipitation (ChIP) assay was performed to analyze the binding of TSC2 promoter and EZH2. The cell apoptosis was evaluated using TUNEL staining and western blot analysis of apoptosis-related proteins. RESULTS: H/R injury increased MALAT1 expression in cardiomyocytes. Furthermore, MALAT1 overexpression inhibited, whereas MALAT1 knockdown enhanced the autophagy of cardiomyocytes. Moreover, MALAT1 overexpression recruited EZH2 to TSC2 promoter regions to elevate H3K27me3 and epigenetically inhibited TSC2 transcription. Importantly, TSC2 overexpression suppressed mTOR signaling and then activated the autophagy. Further results showed that MALAT1 inhibited proliferation and enhanced apoptosis of cardiomyocytes through inhibiting TSC2 and autophagy. CONCLUSION: These findings demonstrate that the increased MALAT1 expression induced by H/R injury enhances cardiomyocyte apoptosis through autophagy inhibition by regulating TSC2-mTOR signaling.
Descritores: Autofagia/fisiologia
Apoptose/fisiologia
Miócitos Cardíacos/metabolismo
Serina-Treonina Quinases TOR/genética
RNA Longo não Codificante/genética
Proteína 2 do Complexo Esclerose Tuberosa/genética
-Autofagia/genética
Transdução de Sinais
Western Blotting
Imunofluorescência
Apoptose/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Imunoprecipitação da Cromatina
Serina-Treonina Quinases TOR/metabolismo
RNA Longo não Codificante/metabolismo
Proteína 2 do Complexo Esclerose Tuberosa/metabolismo
Limites: Animais
Camundongos
Responsável: CL1.1 - Biblioteca Central


  9 / 19 LILACS  
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Id: biblio-1129803
Autor: Ayala González, Diego Armando; Miranda Villasana, José Ernesto; Torres Cruz, Yonatan Josué; Uribe Campos, Alfonso.
Título: Actualización de medicamentos asociados a necrosis avascular de los maxilares: perspectiva y revisión de literatura / Update of medications associated with avascular necrosis of the jaws: a perspective and literature review
Fonte: Rev. ADM = ADM;77(4):197-202, jul.-ago. 2020. tab.
Idioma: es.
Resumo: La osteonecrosis de los maxilares está definida como la exposición de hueso necrótico en la región maxilofacial al menos por ocho semanas en pacientes que están recibiendo medicamentos antirresortivos para el tratamiento del cáncer primario o metastásico hacia el hueso, osteoporosis o enfermedad de Paget, sin historia previa de radiación. Desde el año 2003, la terminología utilizada estaba en relación con los bifosfonatos, en la actualidad ha sido introducido el término osteonecrosis de los maxilares relacionada por medicamentos (OMAM). La cirugía oral (implantología o cirugía periapical) incrementa el riesgo de OMAM, así como los desbalances concomitantes de la salud oral (inflamación dental y formación de abscesos). Las estrategias conservadoras en el tratamiento varían desde el cuidado local conservador hasta la resección quirúrgica radical del hueso necrótico. En el presente artículo se expone un análisis sistemático retrospectivo de la literatura en páginas como PubMed, ScienceDirect y Springer, Cochrane Library. Con el objetivo de resaltar el aumento de la incidencia de OMAM a nivel mundial con el uso de antirresortivos y otros medicamentos asociados en su patogenia en el Hospital Regional «General Ignacio Zaragoza¼ del ISSSTE, UNAM, en la Ciudad de México (AU)

Osteonecrosis of the jaws is defined as the exposure of necrotic bone in the maxillofacial region for at least 8 weeks in patients receiving antiresorptive medications for the treatment of primary or metastatic cancer towards the bone, osteoporosis, or Paget's disease, without previous history of radiation. Since 2003, the terminology used was related to bisphosphonates, the term medication-related osteonecrosis of the jaws has now been introduced. Oral surgery (implantology or periapical surgery) increases the risk of avascular necrosis, as well as concomitant imbalances in oral health (dental inflammation and abscess formation). Conservative strategies in treatment vary from conservative local care to radical surgical resection of the necrotic bone. In this article, a systematic retrospective analysis of the literature is presented on pages such as PubMed, Science Direct and Springer, Cochrane Library. And in which the objective is to highlight the increase in the incidence of medication related osteonecrosis of the jaws worldwide with the use of antiresorptive, and other associated medications in its pathogenesis at the Hospital Regional «General Ignacio Zaragoza¼ ISSSTE, UNAM in Mexico City (AU)
Descritores: Difosfonatos/efeitos adversos
Osteonecrose da Arcada Osseodentária Associada a Difosfonatos
-Osteoporose
Neoplasias Ósseas
Inibidores da Angiogênese
Unidade Hospitalar de Odontologia
Serina-Treonina Quinases TOR
Bevacizumab
Sunitinibe
México
Limites: Humanos
Tipo de Publ: Revisão
Responsável: AR29.1 - Biblioteca


  10 / 19 LILACS  
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Id: biblio-1019508
Autor: Marafie, Sulaiman K; Al-Shawaf, Eman M; Abubaker, Jehad; Arefanian, Hossein.
Título: Palmitic acid-induced lipotoxicity promotes a novel interplay between Akt-mTOR, IRS-1, and FFAR1 signaling in pancreatic ß-cells
Fonte: Biol. Res;52:44, 2019. graf.
Idioma: en.
Projeto: Kuwait Foundation for the Advancement of Sciences (KFAS).
Resumo: BACKGROUND: Free fatty acid receptor 1 (FFAR1) is G-protein coupled receptor predominantly expressed in pancreatic ß-cells that is activated by a variety of free fatty acids (FFAs). Once activated, it promotes glucose-stimulated insulin secretion (GSIS). However, increased levels of FFAs lead to lipotoxicity, inducing loss of ß-cell function. FFAR1 plays a key role in the development of type 2 diabetes (T2D), and previous studies have indicated the importance of developing anti-diabetic therapies against FFAR1, although its role in the regulation of ß-cell function remains unclear. The present study investigated the role of FFAR1 under lipotoxic conditions using palmitic acid (PA). The rat insulinoma 1 clone 832/13 (INS-1 832/13) cell line was used as a model as it physiologically resembles native pancreatic ß-cells. Key players of the insulin signaling pathway, such as mTOR, Akt, IRS-1, and the insulin receptor (INSR1ß), were selected as candidates to be analyzed under lipotoxic conditions. RESULTS: We revealed that PA-induced lipotoxicity affected GSIS in INS-1 cells and negatively modulated the activity of both IRS-1 and Akt. Reduced phosphorylation of both IRS-1 S636/639 and Akt S473 was observed, in addition to decreased expression of both INSR1ß and FFAR1. Moreover, transient knockdown of FFAR1 led to a reduction in IRS-1 mRNA expression and an increase in INSR1ß; mRNA. Finally, PA affected localization of FFAR1 from the cytoplasm to the perinucleus. CONCLUSIONS: In conclusion, our study suggests a novel regulatory involvement of FFAR1 in crosstalk with mTOR-Akt and IRS-1 signaling in ß-cells under lipotoxic conditions.
Descritores: Ácido Palmítico/toxicidade
Receptores Acoplados a Proteínas G/metabolismo
Células Secretoras de Insulina/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Metabolismo dos Lipídeos/efeitos dos fármacos
Serina-Treonina Quinases TOR/metabolismo
-Transdução de Sinais
Linhagem Celular
Apoptose
Células Secretoras de Insulina/metabolismo
Limites: Animais
Ratos
Responsável: CL1.1 - Biblioteca Central



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