Wilms' tumor lncRNA sequence in the blood
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE166606 | GEO | 2021/02/12
REPOSITORIES: GEO
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Project description:Wilms' tumor lncRNA sequence in the blood
| PRJNA701404 | ENA
Project description:We performed a genome-wide analysis of lncRNA expression in hepatoblastoma tissues to identify novel targets for further study of hepatoblastoma.We found that 2736 lncRNAs were differentially expressed in hepatoblastoma tissues. The genome-wide analysis of lncRNA expression in these tissues was performed using a 4 M-CM-^W 180K lncRNA microarray and Sureprint G3 Human lncRNA Chips.Quantitative RT-PCR (qRT-PCR) was performed to confirm these results.
2013-12-31 | E-GEOD-51701 | biostudies-arrayexpress
Project description:Long non-coding RNAs (lncRNAs) have been found to play a role in gene regulation with dysregulated expression in various cancers. The precise role that lncRNA expression plays in the pathogenesis of B-acute lymphoblastic leukemia (B-ALL) is unknown. Therefore, unbiased microarray profiling was performed on human B-ALL specimens and it was determined that lncRNA expression correlates with cytogenetic abnormalities, which was confirmed by RT-qPCR in a large set of B-ALL cases. Importantly, high expression of BALR-2 correlated with poor overall survival and diminished response to prednisone treatment. In line with a function for this lncRNA in regulating cell survival, BALR-2 knockdown led to reduced proliferation, increased apoptosis, and increased sensitivity to prednisolone treatment. Conversely, overexpression of BALR-2 led to increased cell growth and resistance to prednisone treatment. Interestingly, BALR-2 expression was repressed by prednisolone treatment and its knockdown led to upregulation of the glucocorticoid response pathway in both human and mouse B-cells. Together, these findings indicate that BALR-2 plays a functional role in the pathogenesis and/or clinical responsiveness of B-ALL and that altering the levels of particular lncRNAs may provide a future direction for therapeutic development. To define gene expression changes attributable to expression of lncRNAs, we transduced RS4;11 cells with a siRNA against BALR-2 or control vector. These cells were left untreated or treated with prednisolone.
2015-02-05 | E-GEOD-65646 | biostudies-arrayexpress
Project description:Methods and Materials The high throughput RNA sequencing (RNA-seq) data from kidney biopsies of LN patients and controls was applied studied to screen for candidate lncRNAs. Quantitative real-time polymerase chain reaction(RT-qPCR) was used to detect the expression of lncRNAs and individual IFN-stimulated genes (ISGs). Western blotting and dual-luciferace luciferase reporter assay was adopted to explore the specific function of the candidate lncRNA. Results The expression of lncRNA RP11-2B6.2 was significantly increased in the kidney tissues from LN patients compared with those from healthy controls, and positive correlated with the degree of disease activity and renal injuryinjuries. Additionally, expression of LncRNA RP11-2B6.2 could be stimulated by type I IFN. Silencing it RP11-2B6.2 significantly reduced the expression of a group of interferon-stimulating genes(ISGs) including IFIT1, OAS1, etc., Furthermore, it lncRNA RP11-2B6.2 affected the expression of IFN alpha and beta receptor subunit 1 (IFNAR1), phosphorylation of Jak1 and Stat1, and the luciferase activity induced by interferon stimulated response element(ISRE). Conclusion Long noncoding RNA RP11-2B6.2 is a positive regulator of the type I IFN signaling pathway in LN. It LncRNA RP11-2B6.2 may contribute to the pathogenesis of LN and provide served as a potentially therapeutic target.
2019-05-01 | GSE98422 | GEO
Project description:Here, we report the identification of one long noncoding RNA (lncRNA) overexpressed in NPM1-mutated AML patients (named LONA) and whose intracellular localization inversely reflects that of NPM1. LONA overexpression in mutant NPM1 cells inhibits in vitro myeloid differentiation and enhances in vivo tumor growth. LONA overexpression combined with a genome-wide RNA-seq search followed by RT-qPCR validations identified a set of mRNA targets encoding proteins involved in myeloid differentiation (including THSB1, MAFB and ASB2) and in tumor cell apoptosis and interaction with its microenvironment.
2021-06-12 | GSE152351 | GEO
Project description:Two HCT116 cell lines (HCT WT, HCT p21-/-) were analyzed by RT-qPCR array analysis for genes associated with Epithelial to Mesenchymal Transition (EMT) to identify potential target genes, that depend on the cell cycle regulator p21. HCT116 cell lines (HCT WT, HCT p21-/-) were cultured at 37°C in a humidified atmosphere with 5% CO2. Cells were harvested at a confluency of ~60-80% and RNA was isolatd using QIAzol an Rneasy Kits from Qiagen. cDNA was produced from equal amounts of RNA using the RT² First Strand Ki from Qiagen and RT-qPCR analysis was performed following the manufacturer's instructions using the Epithelial to Mesenchymal Transition RT² Profiler PCR Array from Qiagen. The CFX96TM Real-Time System and the C1000TM Thermal Cycler from Bio-Rad were used to perform the RT-PCR runs. The two different cell lines were analyzed in three biological triplicates. The mean expression Ct values of the target genes were normalized against the mean Ct value for B2M to calculate the Fold Change values. The Raw Data was processed using the RT² Profiler PCR Array Data Analysis version 3.5 software from SABiosciences.
2019-12-28 | GSE107665 | GEO
Project description:Three HCT116 cell lines (HCT WT, HCT p21-/-, HCT p53-/-) were analyzed by RT-qPCR array analysis for chromatin modification enzymes to identify potential target genes, that depend on the cell cycle regulator p21 and that are indpendent of p53. HCT116 cell lines (HCT WT, HCT p21-/-, HCT p53-/-) were cultured at 37°C in a humidified atmosphere with 5% CO2. Cells were harvested at a confluency of ~60-80% and RNA was isolatd using QIAzol an Rneasy Kits from Qiagen. cDNA was produced from equal amounts of RNA using the RT² First Strand Ki from Qiagen and RT-qPCR analysis was performed following the manufacturer's instructions using the Epigenetic Chromatin Modification Enzymes RT² Profiler PCR Array from Qiagen. The CFX96TM Real-Time System and the C1000TM Thermal Cycler from Bio-Rad were used to perform the RT-PCR runs. The three different cell lines were analyzed in three biological triplicates. The mean expression Ct values of the target genes were normalized against the mean Ct value for GAPDH to calculate the Fold Change values. The Raw Data was processed using the RT² Profiler PCR Array Data Analysis version 3.5 software from SABiosciences.
2019-12-28 | GSE107664 | GEO
Project description:ArrayStar Human LncRNA/mRNA Expression Microarray Version 3.0 was used to detect lncRNA expression in CRC tissues compared with their matched non-tumoral tissues. Here we report significantly up-regulated as well as down-regulated lncRNAs in CRC tissues compared with their matched non-tumoral tissues.
2019-07-20 | GSE134525 | GEO
Project description:Purpose: we focused on the biological roles and mechanism of the lncRNA LINC00839 in CRC. Methods: In situ hybridization (ISH), and quantitative real-time PCR (qPCR) were used to detect the expression of LINC00839 in paired CRC specimen. Biological function of LINC00839 was determined in vitro and in vivo. Western blot, bioinformatics analysis, RNA pull-down, RNA immunoprecipitation (RIP) and chromatin immunoprecipitation assays (ChIP) were performed to identify the mechanisms underlying the functions of LINC00839 in CRC. Results: We found that LINC00839 was located in the nucleus of CRC cells and that LINC00839 was upregulated in CRC. High expression of LINC00839 was associated with poor outcome in CRC patients. Functionally, upregulation of LINC00839 promoted CRC cell proliferation, invasion, and metastasis in vitro and in vivo. Mechanistic investigations revealed that LINC00839 can promote the acetylation of histones H4K5 and H4K8 at the promoter of NRF1 after recruiting the RUVBL1/Tip60 complex, thereby upregulating the expression of NRF1. Subsequently, NRF1 served as an activator in mitochondrial metabolism and biogenesis, which, in turn, promoted CRC progression.
2022-08-30 | GSE197706 | GEO