1,762,810 research outputs found
AFAP1 antisense RNA 1 promotes retinoblastoma progression by sponging microRNA miR-545-3p that targets G protein subunit beta 1
No full textThe oncogenic role of actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) has been reported in retinoblastoma (RB). However, the underlying regulatory mechanisms remain poorly understood. In this study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting were performed to analyze the expression of AFAP1-AS1, microRNA miR-545-3p, or G protein subunit beta 1 (GNB1). Cell Counting Kit-8 (CCK-8) and Transwell migration assays were used to detect cell proliferation and migration. In addition, caspase-3 activity was monitored by caspase-3 activity assay. Luciferase reporter assays combined with RNA immunoprecipitation (RIP) and pull-down assays were performed to elucidate the target relationship between miR-545-3p and AFAP1-AS1 or GNB1. Xenograft tumor experiments were performed to evaluate RB cell growth in vivo. Increased AFAP1-AS1 and GNB1 expression in RB tissues and cells was confirmed by RT-qPCR; conversely, miR-545-3p was found to be downregulated in RB tissues and cells. AFAP1-AS1 overexpression resulted in increased proliferation and migration of RB cells, whereas AFAP1-AS1 silencing resulted in decreased proliferation and migration of RB cells. Moreover, AFAP1-AS1 was found to target miR-545-3p. The anti-miR-545-3p treatment phenocopied the effect of AFAP1-AS1 overexpression and promoted RB cell growth in vivo. miR-545-3p was found to directly target GNB1. GNB1 silencing resulted in reduced proliferation and migration of RB cells and attenuated the oncogenic effect of the miR-545-3p inhibitor. Thus, in this study, a novel ceRNA regulation network of AFAP1-AS1 in RB was identified, where AFAP1-AS1 regulated GNB1 expression by targeting miR-545-3p, ultimately driving RB progression.</p
Circ_0072008, an oncogene in pancreatic ductal adenocarcinoma, contributes to tumour cell malignant progression and glycolysis by regulating miR-545-3p/SLC7A11 axis
No full textThe hsa_circRNA_103809 (circ_0072088) has been an emerging tumour regulator in human cancers, and is identified as one most aberrantly expressed circRNA in patients with pancreatic ductal adenocarcinoma (PDAC). However, the role of circ_0072088 remains unclear in PDAC cells. Expression of circ_0072088, microRNA (miR)-545-3p and solute carrier family 7 member 11 (SLC7A11) was detected by real-time quantitative PCR and western blotting. Cell progression was measured by cell counting kit (CCK)-8 assay, transwell assays and flow cytometry, as well as xenograft tumour models. Glycolysis was evaluated by commercial assay kits. The interaction among circ_0072088, miR-545-3p and SLC7A11 was confirmed by dual-luciferase reporter assay. Circ_0072088 was upregulated in PDAC tumours and cells; besides, high circ_0072088 level was associated with high tumour-node-metastasis (TNM) stage. The circ_0072088 siRNA suppressed cell viability, migration, invasion, extracellular acidification rate (ECAR), lactate production, glucose uptake, and ATP generation, but promoted apoptosis rate and oxygen consumption rate (OCR) in SW1990 and PANC-1 cells. In vivo, circ_0072088 knockdown retarded tumour growth of PANC-1 cells. Overexpressing miR-545-3p mimicked circ_0072088 siRNA-induced actions, and inhibited cell progression and glycolysis of SW1990 and PANC-1 cells. Moreover, SLC7A11 downregulation could be mediated by both circ_0072008 siRNA and miR-545-3p mimic, and participating in suppressive role in cell progression and glycolysis of SW1990 and PANC-1 cells. In mechanism, miR-545-3p was targeted by circ_0072008, and SLC7A11 was target of miR-545-3p. Circ_0072088 elicited oncogenic role in malignant cell progression and glycolysis of PDAC cells through circ_0072088/miR-545-3p/SLC7A11 pathway.HighlightsCirc_0072088 was upregulated in PDAC tumours and was associated with high tumour burden.Blocking circ_0072088 suppressed cell proliferation, migration, invasion, and glycolysis in PDAC cells.Circ_0072088 could directly regulate miR-545-3p, and SLC7A11 was a target of miR-545-3p.Restoring miR-545-3p mimicked the effects of circ_0072088 knockdown in PDAC cell in vitro. Circ_0072088 was upregulated in PDAC tumours and was associated with high tumour burden. Blocking circ_0072088 suppressed cell proliferation, migration, invasion, and glycolysis in PDAC cells. Circ_0072088 could directly regulate miR-545-3p, and SLC7A11 was a target of miR-545-3p. Restoring miR-545-3p mimicked the effects of circ_0072088 knockdown in PDAC cell in vitro.</p
Long non-coding RNA CASC9 promotes tumor progression in oral squamous cell carcinoma by regulating microRNA-545-3p/laminin subunit gamma 2
No full textLong non-coding RNA (lncRNA) CASC9 is reported to be a tumor promoter in oral cancer, but its mechanism in oral squamous cell carcinoma (OSCC) has not been fully explored. Our study aimed to identify the interaction between lncRNA CASC9, microRNA-545-3p (miR-545-3p), and laminin subunit gamma 2 (LAMC2) in OSCC cells. Our study confirmed that lncRNA CASC9 and LAMC2 were upregulated in OSCC, whereas miR-545-3p expression was reduced. After performing a series of cell functional experiments, it was found that knockdown of lncRNA CASC9 or LAMC2 resulted in the inhibition of proliferation, colony formation, and migration of OSCC cells, but their negative effects could be partly impaired by the miR-545-3p inhibitor. In addition, we proved for the first time that lncRNA CASC9 can sponge miR-545-3p to upregulate LAMC2. In conclusion, our study revealed that lncRNA CASC9 promotes the malignancy of OSCC cells by sponging miR-545-3p to enhance LAMC2 expression, implying that lncRNA CASC9/miR-545-3p/LAMC2 may be an intervention approach in OSCC therapy.</p
Additional file 1 of Circ_0072083 interference enhances growth-inhibiting effects of cisplatin in non-small-cell lung cancer cells via miR-545-3p/CBLL1 axis
No full textAdditional file 1: Figure S1. The influence of DDP, circ_0072083, miR-545-3p and CBLL1 on the necrosis of NSCLC cells. a The viability of NSCLC cells treated with si-NC, si-circ_0072083, DDP + si-NC or DDP + si-circ_0072083 was detected by LDH cytotoxicity assay kit. b LDH cytotoxicity assay kit was used to measure the necrosis of DDP-induced NSCLC cells transfected with si-NC, si-circ_0072083, si-circ_0072083 + anti-miR-NC or si-circ_0072083 + anti-miR-545-3p. c The viability of DDP-treated NSCLC cells transfected with miR-NC, miR-545-3p, miR-545-3p + vector or miR-545-3p + CBLL1 was determined through using LDH cytotoxicity assay kit. *P < 0.05
Image_1_The Circ_0001367/miR-545-3p/LUZP1 Axis Regulates Cell Proliferation, Migration and Invasion in Glioma Cells.tif
No full textGlioma is the most common primary intracranial malignant tumour in adults. It has a high incidence and poses a serious threat to human health. Circular RNA is a hotspot of cancer research. In this study, we aimed to explore the role of circ_0001367 in gliomagenesis and the underlying mechanism. First, qRT-PCR was conducted, which showed that circ_0001367 level was downregulated in glioma tissues and cells. Next, gain-of-function and loss-of-function assays were performed, which indicated that circ_0001367 inhibited the proliferation, migration and invasion of glioma cells. Subsequent bioinformatics analysis, dual-luciferase reporter assays, RNA immunoprecipitation assays and cell function assays demonstrated that circ_0001367 inhibited the proliferation, migration and invasion of glioma cells by absorbing miR-545-3p and thereby regulating the expression of leucine zipper protein (LUZP1). Finally, an in vivo experiment was conducted, which demonstrated that circ_0001367 inhibited glioma growth in vivo by modulating miR-545-3p and LUZP1. Taken together, the results of this study demonstrate that the circ_0001367/miR-545-3p/LUZP1 axis may be a novel target for glioma therapy.</p
Image_2_The Circ_0001367/miR-545-3p/LUZP1 Axis Regulates Cell Proliferation, Migration and Invasion in Glioma Cells.tif
No full textGlioma is the most common primary intracranial malignant tumour in adults. It has a high incidence and poses a serious threat to human health. Circular RNA is a hotspot of cancer research. In this study, we aimed to explore the role of circ_0001367 in gliomagenesis and the underlying mechanism. First, qRT-PCR was conducted, which showed that circ_0001367 level was downregulated in glioma tissues and cells. Next, gain-of-function and loss-of-function assays were performed, which indicated that circ_0001367 inhibited the proliferation, migration and invasion of glioma cells. Subsequent bioinformatics analysis, dual-luciferase reporter assays, RNA immunoprecipitation assays and cell function assays demonstrated that circ_0001367 inhibited the proliferation, migration and invasion of glioma cells by absorbing miR-545-3p and thereby regulating the expression of leucine zipper protein (LUZP1). Finally, an in vivo experiment was conducted, which demonstrated that circ_0001367 inhibited glioma growth in vivo by modulating miR-545-3p and LUZP1. Taken together, the results of this study demonstrate that the circ_0001367/miR-545-3p/LUZP1 axis may be a novel target for glioma therapy.</p
Resolución UNRN N° 545/2009. Aprobar la designación del personal docente universitario
No full textFil: Universidad Nacional de Río Negro (U). Universidad Nacional de Río Negro. Río Negro, ArgentinaResolución UNRN N° 545/2009. Aprobar la designación del personal docente universitariofals
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
El Tlacuache Núm. 545 (2012). 545 Año 13 (2012) noviembre. El Tlacuache
No full text¿Nuevo escudo morelense? por Carlos Barreto Mark. -Las piedras no hablan solas por Omar Espinosa Severino. -La migración en la tradición indígena en Morelos por Luis Miguel Morayta Mendoza. -El mito de Quetzacóatl en Amatlán, Morelos por Erick Alvarado Tenorio, Xochitl Zambrano Bernal
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