× Atenção: Esta versão do sistema de pesquisa será desativada em 01/12/2022. Recomendamos a utilização da nova versão disponível em pesquisa.bvsalud.org


Base de dados : LILACS
Pesquisa : D12.776.157.725 [Categoria DeCS]
Referências encontradas : 38 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 4 ir para página            

  1 / 38 LILACS  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Chile
Texto completo
Id: biblio-950853
Autor: Zhao, Xiaolan; Chen, Man; Tan, Jishan.
Título: Knockdown of ZFR suppresses cell proliferation and invasion of human pancreatic cancer
Fonte: Biol. Res;49:1-8, 2016. ilus, graf.
Idioma: en.
Resumo: BACKGROUND: Zinc finger RNA binding protein (ZFR) is involved in the regulation of growth and cancer development. However, little is known about ZFR function in pancreatic cancer. METHODS: Herein, to investigate whether ZFR is involved in tumor growth, Oncomine microarray data was firstly used to evaluate ZFR gene expression in human pancreatic tumors. Then short hairpin RNA (shRNA) targeting ZFR was designed and delivered into PANC-1 pancreatic cancer cells to knock down ZFR expression. Cell viability, cell proliferation and cell cycle analysis after ZFR knockdown were determined by MTT, colony forming and FACS, respectively. In addition, cell migration and invasion were assessed using the Transwell system. RESULTS: The expression of ZFR was significantly higher in pancreatic tumors than normal pancreas tissues by Oncomine database analysis. Knockdown of ZFR by shRNA-expressing lentivirus significantly decreased the viability and invasion ability of pancreatic cancer cells. Moreover, FACS analysis showed that knockdown of ZFR in PANC-1 cells caused a significant cell cycle arrest at G0/G1 phase. Furthermore, knockdown of ZFR decreased the levels of CDK2, CDK4, CyclinA and CyclinD1 and enhanced the expression of p27, which has evidenced by qRT-PCR and Western blot analysis. CONCLUSIONS: Knockdown of ZFR might provide a novel alternative to targeted therapy of pancreatic cancer and deserves further investigation.
Descritores: Neoplasias Pancreáticas/patologia
Proteínas de Ligação a RNA/metabolismo
RNA Interferente Pequeno/farmacologia
Técnicas de Silenciamento de Genes/métodos
-Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/metabolismo
Sais de Tetrazólio
Sobrevivência Celular
Células Cultivadas
Western Blotting
Proteínas de Ligação a RNA/genética
Lentivirus/genética
Linhagem Celular Tumoral
Proliferação de Células/genética
Terapia de Alvo Molecular
Reação em Cadeia da Polimerase em Tempo Real
Citometria de Fluxo/métodos
Formazans
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Limites: Animais
Bovinos
Humanos
Responsável: BR1.1 - BIREME


  2 / 38 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Texto completo
Texto completo
Id: biblio-1350611
Autor: Liu, Xiaojuan; Ma, Hui; Ma, Lisha; Li, Kun; Kang, Yanhua.
Título: RNA-binding protein with serine-rich domain 1 regulates microsatellite instability of uterine corpus endometrial adenocarcinoma
Fonte: Clinics;76:e3318, 2021. tab, graf.
Idioma: en.
Resumo: OBJECTIVE: To determine the role of RNA-binding protein with serine-rich domain 1 (RNPS1) in uterine corpus endometrial carcinoma (UCEC), the role of RNPS1 knockdown in UCEC development in vitro and in vivo, and the relationship between RNPS1 and mismatch repair (MMR) in UCEC. METHODS: We predicted the potential function of RNPS1 using bioinformatics systems. The expression of RNPS1 in tissues and cell lines was analyzed by western blotting and immunohistochemistry. The expression of RNPS1 in MMR was assessed using bioinformatics and western blotting. The proliferation and apoptosis of UCEC cells were assessed under RNPS1 knockdown conditions, and RNPS1 regulation in MMR was detected by suppressing Notch signaling. Associations between RNPS1 and gene mutations in UCEC and prognosis were analyzed. RESULTS: The RNPS1 level was higher in UCEC tumors than in normal tissues and tumors or RL952 cells. Prognostic outcomes were worse when UCEC showed abundant RNPS1 expression. Lentiviral RNPS1 knockdown weakened tumor cell proliferation and suppressed biomarker expression, reduced the tumor volume, promoted apoptosis in vitro and in vivo, and inhibited UCEC development. Increased MutS homolog 2 (MSH2) and MutS homolog 6 (MSH6) levels in MMR after RNPS1 knockdown were reversed by inhibiting Notch signaling. Furthermore, RNPS1 was associated with mutations in NAA11, C2orf57, NUPR1, and other genes involved in UCEC prognosis. CONCLUSION: RNPS1 may regulate the expression levels of MSH2 and MSH6 in MMR, enhancing the proliferation, development, and prognosis of UCEC through a Notch signaling pathway in UCEC. Our study offers a new method and strategy for delaying UCEC development through modulating MMR.
Descritores: Ribonucleoproteínas/genética
Neoplasias do Endométrio/genética
Carcinoma Endometrioide/congênito
-Serina
Proteínas de Ligação a RNA
Linhagem Celular Tumoral
Instabilidade de Microssatélites
Limites: Humanos
Feminino
Responsável: BR1.1 - BIREME


  3 / 38 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Saúde Pública
Texto completo
Id: lil-793000
Autor: Pineda-Belmontes, Cristina P; Hernández-Ramírez, Raúl U; Hernández-Alcaraz, César; Cebrián, Mariano E; López-Carrillo, Lizbeth.
Título: Genetic polymorphisms of PPAR gamma, arsenic methylation capacity and breast cancer risk in Mexican women / Polimorfismos genéticos de PPAR gamma, capacidad de metilación del arsénico y riesgo de cáncer de mama en mujeres mexicanas
Fonte: Salud pública Méx;58(2):220-227, Mar.-Apr. 2016. tab.
Idioma: en.
Projeto: National Science and Technology Council (Consejo Nacional de Ciencia y Tecnología - Conacyt); . Sectorial Fund for Research in Health and Safety (Fondo Sectorial de Investigación en Salud y Seguridad.
Resumo: Abstract Objective: To evaluate whether the presence of polymorphisms of peroxisome proliferator-activated receptor gamma PPARγ (Pro 1 2Ala) and PPARGC1B (Ala203Pro) modifies the association between the inorganic arsenic (iAs) methylation capacity and breast cancer (BC). Materials and methods: Mexican women were interviewed, and blood and urine samples were collected from them (cases/controls= 197/220). The concentration of urinary arsenic species and the polymorphisms of interest were determined by high-performance liquid chromatography with inductively coupled plasma mass spectrometry (HPLC-ICP-MS) and polymerase chain reaction (PCR), respectively. Results: In women with a high %MMA (urinary monomethyl arsenic) and high primary methylation ratio (PM = MMA/iAs), the risk of BC was increased (odds ratio [OR]%MMA T3 vs.T1= 3.60: 95% confidence interval [CI] 2.02-6.41, ORPMI T3 vs.T1= 3.47: 95%CI 1.95-6.17), which was maintained after adjusting for polymorphisms. No significant interactions were observed between the polymorphisms and the arsenic variables on the risk of BC. Conclusion: Pro 12Ala and Ala203Pro polymorphisms did not modify the association between the iAs methylation capacity and BC.

Resumen Objetivo: Evaluar si la presencia de polimorfismos de PPARγ (Pro 1 2Ala) y PPARGC1B (Ala203Pro) modifica la asociación entre la capacidad de metilación del arsénico inorgánico (Asi) y el cáncer de mama (CM). Material y métodos: Se entrevistaron mujeres mexicanas y recolectaron muestras de sangre y orina de (casos/controles=197/220). La concentración de especies de arsénico urinario y los polimorfismos de interés se determinaron mediante cromatografía líquida de alta resolución acoplada a espectrometría de masas (HPLC-ICP-MS) y reacción en cadena de la polimerasa (PCR), respectivamente. Resultados: En mujeres con %MMA (monometilarsénico urinario) y razón de primera metilación altas (PM=MMA/Asi) se incrementó el riesgo de CM (RM%MMAT3vsT1=3.60: intervalo de confianza [IC]95%2.02-6.41, RMPMT3vs.T1=3.47:IC95%1.95-6.17), que se mantuvo, respectivamente, al ajustar por polimorfismos. No se observaron interacciones significativas entre los polimorfismos y las variables arsenicales sobre el riesgo de CM. Conclusión: Los polimorfismos Pro 12Ala y Ala203Pro no modificaron la asociación entre la capacidad de metilación del Asi y el CM.
Descritores: Arsenicais/metabolismo
Neoplasias da Mama/epidemiologia
Proteínas de Transporte/genética
Polimorfismo de Nucleotídeo Único
PPAR gama/genética
-Arsênio/toxicidade
Arsenicais/urina
Espectrometria de Massas
Neoplasias da Mama/genética
Estudos de Casos e Controles
Reação em Cadeia da Polimerase
Risco
Cromatografia Líquida de Alta Pressão
Proteínas de Ligação a RNA
Predisposição Genética para Doença
Exposição Ambiental
Metilação
Limites: Humanos
Feminino
Adulto
Pessoa de Meia-Idade
Idoso
Adulto Jovem
Responsável: BR1.1 - BIREME


  4 / 38 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Romanha, Alvaro José
Texto completo
Id: biblio-1040603
Autor: Moreira, Douglas de Souza; Duarte, Ana Paula; Pais, Fabiano Sviatopolk Mirsky; Silva-Pereira, Rosiane Aparecida da; Romanha, Alvaro José; Schenkman, Sergio; Murta, Silvane Maria Fonseca.
Título: Overexpression of eukaryotic initiation factor 5A (eIF5A) affects susceptibility to benznidazole in Trypanosoma cruzi populations
Fonte: Mem. Inst. Oswaldo Cruz;113(9):e180162, 2018. graf.
Idioma: en.
Projeto: AJR; . SS; . SMFM; . DSM; . CNPq; . DSM; . APD.
Resumo: Eukaryotic initiation factor 5A (eIF5A) is a conserved protein with an essential role in translation elongation. Using one and two-dimensional western blotting, we showed that the eIF5A protein level was 2-fold lower in benznidazole (BZ)-resistant (BZR and 17LER) Trypanosoma cruzi populations than in their respective susceptible counterparts (BZS and 17WTS). To confirm the role of eIF5A in BZ resistance, we transfected BZS and 17WTS with the wild-type eIF5A or mutant eIF5A-S2A (in which serine 2 was replaced by alanine). Upon overexpressing eIF5A, both susceptible lines became approximately 3- and 5-fold more sensitive to BZ. In contrast, the eIF5A-S2A mutant did not alter its susceptibility to BZ. These data suggest that BZ resistance might arise from either decreasing the translation of proteins that require eIF5A, or as a consequence of differential levels of precursors for the hypusination reactions (e.g., spermidine and trypanothione), both of which alter BZ's effects in the parasite.
Descritores: Tripanossomicidas/farmacologia
Trypanosoma cruzi/efeitos dos fármacos
Trypanosoma cruzi/enzimologia
Resistência a Medicamentos/genética
Fatores de Iniciação de Peptídeos/metabolismo
Proteínas de Ligação a RNA/metabolismo
Nitroimidazóis/farmacologia
-Trypanosoma cruzi/genética
Expressão Gênica
Fatores de Iniciação de Peptídeos/análise
Fatores de Iniciação de Peptídeos/efeitos dos fármacos
Proteínas de Ligação a RNA/análise
Proteínas de Ligação a RNA/efeitos dos fármacos
Limites: Humanos
Responsável: BR1.1 - BIREME


  5 / 38 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-951681
Autor: Chen, B; Huang, S G; Ju, L; Li, M; Nie, F F; Zhang, Y; Zhang, Y H; Chen, X; Gao, F.
Título: Effect of microRNA-21 on the proliferation of human degenerated nucleus pulposus by targeting programmed cell death 4
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;49(6):e5020, 2016. tab, graf.
Idioma: en.
Resumo: This study aims to explore the effect of microRNA-21 (miR-21) on the proliferation of human degenerated nucleus pulposus (NP) by targeting programmed cell death 4 (PDCD4) tumor suppressor. NP tissues were collected from 20 intervertebral disc degeneration (IDD) patients, and from 5 patients with traumatic spine fracture. MiR-21 expressions were tested. NP cells from IDD patients were collected and divided into blank control group, negative control group (transfected with miR-21 negative sequences), miR-21 inhibitor group (transfected with miR-21 inhibitors), miR-21 mimics group (transfected with miR-21 mimics) and PDCD4 siRNA group (transfected with PDCD4 siRNAs). Cell growth was estimated by Cell Counting Kit-8; PDCD4, MMP-2,MMP-9 mRNA expressions were evaluated by qRT-PCR; PDCD4, c-Jun and p-c-Jun expressions were tested using western blot. In IDD patients, the expressions of miR-21 and PDCD4 mRNA were respectively elevated and decreased (both P<0.05). The miR-21 expressions were positively correlated with Pfirrmann grades, but negatively correlated with PDCD4 mRNA (both P<0.001). In miR-21 inhibitor group, cell growth, MMP-2 and MMP-9 mRNA expressions, and p-c-Jun protein expressions were significantly lower, while PDCD4 mRNA and protein expressions were higher than the other groups (all P<0.05). These expressions in the PDCD4 siRNA and miR-21 mimics groups was inverted compared to that in the miR-21 inhibitor group (all P<0.05). MiR-21 could promote the proliferation of human degenerated NP cells by targeting PDCD4, increasing phosphorylation of c-Jun protein, and activating AP-1-dependent transcription of MMPs, indicating that miR-21 may be a crucial biomarker in the pathogenesis of IDD.
Descritores: Proteínas de Ligação a RNA/metabolismo
MicroRNAs/metabolismo
Proliferação de Células/fisiologia
Proteínas Reguladoras de Apoptose/metabolismo
Núcleo Pulposo/metabolismo
-Valores de Referência
Fatores de Tempo
Proteínas Reguladoras de Apoptose/análise
Limites: Humanos
Masculino
Feminino
Adulto
Pessoa de Meia-Idade
Idoso
Responsável: BR1.1 - BIREME


  6 / 38 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-1089356
Autor: Lv, Xinting; Cheng, Huifei.
Título: Prognostic value of increased expression of RBM8A in gastric cancer
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;53(4):e9290, 2020. tab, graf.
Idioma: en.
Resumo: This study was designed to investigate the expression of RBM8A protein in patients with gastric cancer (GC) and to explore its correlation with clinical pathological features as well as prognosis. One hundred pairs of gastric carcinoma tissues and adjacent tissues from patients undergoing gastrectomy for GC were included in this study. The protein expression level of RBM8A was determined by immunohistochemistry using tissue microarrays. We also detected the mRNA expression level of RBM8A in 16 pairs of gastric carcinoma tissues and adjacent tissues. Meanwhile, we predicted the potential correlation between RBM8A and tumor stages as well as survival condition in patents with GC based on The Cancer Genome Atlas (TCGA) database. The correlation of RBM8A with the clinical pathological features and prognosis of the 100 patients with GC was also elucidated. The expression level of RBM8A was significantly higher in gastric carcinoma tissues compared to the adjacent tissues. The protein level of RBM8A was correlated with tumor size (P=0.031), depth of invasion (P<0.001), lymph node metastasis (P<0.001), TNM stage (<0.001), and distant metastasis (P=0.001). Patients with increased RBM8A expression (P<0.0018, 95%CI=0.322−0.871), higher TNM stage (P<0.001, 95%CI=4.990−11.283), and lymph node metastasis (P<0.001, 95%CI=2.873−4.002) had a lower overall survival. Taken together, our study demonstrated that RBM8A may act as a proto-oncogene, which could be a promising biomarker and therapeutic target in the diagnosis and treatment of GC.
Descritores: Neoplasias Gástricas/metabolismo
Proteínas de Ligação a RNA/metabolismo
-Prognóstico
Neoplasias Gástricas/genética
Neoplasias Gástricas/patologia
RNA Mensageiro/metabolismo
Imuno-Histoquímica
Biomarcadores Tumorais/genética
Regulação Neoplásica da Expressão Gênica
Análise de Sobrevida
Proteínas Proto-Oncogênicas/metabolismo
Proteínas de Ligação a RNA/genética
Mucosa Gástrica/patologia
Metástase Linfática/patologia
Metástase Neoplásica
Estadiamento de Neoplasias
Limites: Humanos
Masculino
Feminino
Adulto
Pessoa de Meia-Idade
Idoso
Idoso de 80 Anos ou mais
Responsável: BR1.1 - BIREME


  7 / 38 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-1285646
Autor: Wan, Jiajin; Niu, Chunling; Wang, Baiyan; Han, Qianqian; Chen, Yulon; Feng, Shuying; Yang, Lianhe.
Título: Human esophageal fibroblast-derived exosomal miR-21 reduced the cisplatin sensitivity to esophageal carcinoma EC9706 cells
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;54(10):e11156, 2021. graf.
Idioma: en.
Projeto: Key Science and Technology Research Project of Henan Province of China; . Key Scientific Research Project in Colleges and Universities of Henan Province of China.
Resumo: The objective of this study was to investigate the effect of human esophageal fibroblast-derived exosomal miR-21 on cisplatin sensitivity against esophageal squamous EC9706 cells. EC9706 cells were co-cultured indirectly with human esophageal fibroblasts (HEF) or miR-21 mimics transfected-HEF in the transwell system. The exosomes in HEF-culture conditioned medium were extracted by differential ultracentrifugation. EC9706 cells were co-cultured with HEF-derived exosomes directly. The cisplatin sensitivity against EC9706 cells was revealed via half maximal inhibitory concentration (IC50) values using MTT assay. The expressions of miR-21, programmed cell death 4 (PDCD4) mRNA, and gene of phosphate and tension homology deleted on chromosome ten (PTEN) mRNA were determined by qRT-PCR. The changes of the protein level were detected using western blot assay. IC50 values of cisplatin against EC9706 cells were increased after EC9706 cells were co-cultured with either HEF or exosomes derived from miR-21 mimics-transfected HEF. Following the increased level of miR-21, the mRNA expression and protein levels of PTEN and PDCD4 were decreased in EC9706 cells. The cisplatin sensitivity to EC9706 cells was reduced by HEF-derived exosomal miR-21 through targeting PTEN and PDCD4. This study suggested that non-tumor cells in the tumor micro-environment increased the tumor anti-chemotherapy effects through their exosomes.
Descritores: Neoplasias Esofágicas/genética
Neoplasias Esofágicas/tratamento farmacológico
Carcinoma
MicroRNAs/genética
-Cisplatino/farmacologia
Proteínas de Ligação a RNA
Apoptose
Linhagem Celular Tumoral
Proliferação de Células
Proteínas Reguladoras de Apoptose/metabolismo
Microambiente Tumoral
Fibroblastos/metabolismo
Limites: Humanos
Responsável: BR1.1 - BIREME


  8 / 38 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
Id: biblio-1223212
Autor: Wu, Haiying; Li, Sijie; Ji, Minghua; Chen, Qiao; Shi, Jiping; Blamey, Jenny M; Sun, Junsong.
Título: Improvement of polyhydroxybutyrate production by deletion of csrA in Escherichia coli
Fonte: Electron. j. biotechnol;46:8-13, jul. 2020. tab, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China.
Resumo: BACKGROUND: Poly-3-hydroxybutyrate (PHB) can be efficiently produced in recombinant Escherichia coli by the overexpression of an operon (NphaCAB) encoding PHB synthetase. Strain improvement is considered to be one of critical factors to lower the production cost of PHB in recombinant system. In this study, one of key regulators that affect the cell growth and PHB content was confirmed and analyzed. RESULT: S17-3, a mutant E. coli strain derived from S17-1, was found to be able to achieve high cell density when expressing NphaCAB with the plasmid pBhya-CAB. Whole genome sequencing of S17-3 revealed genetic alternations on the upstream regions of csrA, encoding a global regulator cross-talking between stress response, catabolite repression and other metabolic activities. Deletion of csrA or expression of mutant csrA resulted in improved cell density and PHB content. CONCLUSION: The impact of gene deletion of csrA was determined, dysfunction of the regulators improved the cell density of recombinant E. coli and PHB production, however, the detail mechanism needs to be further clarified.
Descritores: Escherichia coli/metabolismo
Hidroxibutiratos/metabolismo
-Proteínas Repressoras/genética
Biopolímeros/genética
Proteínas Recombinantes
Proteínas de Ligação a RNA/genética
Deleção de Genes
Proteínas de Escherichia coli/genética
Escherichia coli/genética
Engenharia Metabólica
Ligases/metabolismo
Responsável: CL1.1 - Biblioteca Central


  9 / 38 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-892928
Autor: Yang, Zhi-Gang; Ma, Xu-Dong; He, Zhao-Hui; Guo, Ying-xin.
Título: miR-483-5p promotes prostate cancer cell proliferation and invasion by targeting RBM5
Fonte: Int. braz. j. urol;43(6):1060-1067, Nov.-Dec. 2017. graf.
Idioma: en.
Resumo: ABSTRACT Objective: miR-483-5p has been identified as a miRNA oncogene in certain cancers. However, its role in prostate cancer has not been sufficiently investigated. In this study, we investigated the role of miR-483-5p in prostate cancer and examined RBM5 regulation by miR-483-5p. Material and methods: Expression levels of miR-483-5p were determined by quantitative real-time PCR. The effect of miR-483-5p on proliferation was evaluated by MTT assay, cell invasion was evaluated by trans-well invasion assays, and target protein expression was determined by western blotting in LNCaP, DU-145, and PC-3 cells. Luciferase reporter plasmids were constructed to confirm the action of miR-483-5p on downstream target gene RBM5 in HEK-293T cells. Results: we observed that miR-483-5p was upregulated in prostate cancer cell lines and tissues. A miR-483-5p inhibitor inhibited prostate cancer cell growth and invasion in DU-145 and PC-3 cells. miR-483-5p directly bound to the 3' untranslated region (3'UTR) of RBM5 in HEK-293T cells. RBM5 overexpression inhibited prostate cancer cell growth and invasion in LNCaP cells. Enforced RBM5 expression alleviated miR-483-5p promotion of prostate cancer cell growth and invasion in LNCaP cells. Conclusion: The present study describes a potential mechanism underlying a miR-483-5p/RBM5 link that contributes to prostate cancer development.
Descritores: Neoplasias da Próstata/genética
Neoplasias da Próstata/patologia
Regulação Neoplásica da Expressão Gênica/genética
Proteínas de Ciclo Celular/metabolismo
Regiões não Traduzidas/genética
Proteínas Supressoras de Tumor/metabolismo
MicroRNAs/fisiologia
Proliferação de Células/genética
Proteínas de Ligação a DNA/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
-Neoplasias da Próstata/mortalidade
Regulação para Baixo
Regulação para Cima
Proteínas de Ligação a RNA/metabolismo
MicroRNAs/antagonistas & inibidores
Linhagem Celular Tumoral
Invasividade Neoplásica
Limites: Humanos
Masculino
Responsável: BR1.1 - BIREME


  10 / 38 LILACS  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Chile
Texto completo
Id: biblio-1131887
Autor: Cao, Danxia; Zhu, Han; Zhao, Qian; Huang, Jianming; Zhou, Cixiang; He, Jianrong; Liang, Yongjun.
Título: MiR-128 suppresses metastatic capacity by targeting metadherin in breast cancer cells
Fonte: Biol. Res;53:43, 2020. tab, graf.
Idioma: en.
Projeto: Pudong Bureau of Health and Family Planning; . National Science Foundation of China.
Resumo: BACKGROUND: Breast cancer, the most common cancer in women worldwide, causes the vast majority of cancer-related deaths. Undoubtedly, tumor metastasis and recurrence are responsible for more than 90 percent of these deaths. MicroRNAs are endogenous noncoding RNAs that have been integrated into almost all the physiological and pathological processes, including metastasis. In the present study, the role of miR-128 in breast cancer was investigated. RESULTS: Compared to the corresponding adjacent normal tissue, the expression of miR-128 was significantly suppressed in human breast cancer specimens. More importantly, its expression level was reversely correlated to histological grade of the cancer. Ectopic expression of miR-128 in the aggressive breast cancer cell line MDA-MB-231 could inhibit cell motility and invasive capacity remarkably. Afterwards, Metadherin (MTDH), also known as AEG-1 (Astrocyte Elevated Gene 1) and Lyric that implicated in various aspects of cancer progression and metastasis, was further identified as a direct target gene of miR-128 and its expression level was up-regulated in clinical samples as expected. Moreover, knockdown of MTDH in MDA-MB-231 cells obviously impaired the migration and invasion capabilities, whereas re-expression of MTDH abrogated the suppressive effect caused by miR-128. CONCLUSIONS: Overall, these findings demonstrate that miR-128 could serve as a novel biomarker for breast cancer metastasis and a potent target for treatment in the future.
Descritores: Neoplasias da Mama/genética
MicroRNAs/fisiologia
MicroRNAs/genética
Invasividade Neoplásica/genética
-Moléculas de Adesão Celular/genética
Moléculas de Adesão Celular/metabolismo
Regulação Neoplásica da Expressão Gênica
Proteínas de Ligação a RNA
Linhagem Celular Tumoral
Proteínas de Membrana
Recidiva Local de Neoplasia
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central



página 1 de 4 ir para página            
   


Refinar a pesquisa
  Base de dados : Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde
WXIS|fatal error|unavoidable|recxref/read|