Effect of overexpression of NFAT5 on gene expression during TMZ resistance of U87 and U251 cells.
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PROVIDER: PRJNA898426 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the mechanism of NFAT5 resistance to TMZ in gliomas, we performed mRNA sequencing analysis of NFAT5-overexpressing U251 and U87 cell lines.
2023-06-18 | GSE217347 | GEO
Project description:The objective of the study was to examine the gene expression changes in glioma cell line U87 and U251 with LAMP2A knockdown. There were 15 samples in total- U87-1, U87-2, U87-3, U87-1812-1, U87-1812-2, U87-1812-3, U251-1, U251-2, U251-3, U251-1812-1, U251-1812-2, U251-1812-3, U251-1813-1, U251-1813-2, and U251-1813-3. U87-1 to U87-3 and U251--1 to U251-3 were used as the control groups (CON). U87-1812-1 to U871812-3, U251-1812-1 to U251-1812-3, and U251-1813-1 to U251-1813-3 were used as the experimental groups (shLAMP2A-1 and shLAMP2A-2). The total RNA of each sample was extracted from the stable transfected glioma cells by using TRIzol reagent. Then the RNA samples were processed for high throughput transcriptome sequencing on Illumina HiSeq 3000 platform. There were two types of libraries: the circRNA, mRNA, and lncRNA were all constructed by removing rRNA (one library, three types of RNA were analyzed together), and the insert fragment was about 300bp; the small RNA was constructed and analyzed separately, mainly microRNA of about 22bp. Results: among 60612 cleaned mRNAs, 781 were differentially expressed in U87-1812 group compared with U87 group, 146 were differentially expressed in U251-1812 group compared with U251 group, 43 were differentially expressed in U251-1813 group compared with U251 group (padj ≤ 0.05 and expression change ≥2 fold). The differential expressed genes distributed in all chromosomes. Functional annotation with GO and KEGG enrichment revealed the top functional groups including inflammation, DNA replication, cell adhesion, TNF, IL17, and axon guidance signaling pathways.
2024-07-15 | GSE270618 | GEO
Project description:We present RNA-Seq data obtained from U251 control cells and U251 cells with stable overexpression of lncRNA XLOC13218 to identify differentially expressed genes. The discovery of long non-coding RNAs (lncRNAs) has improved the understanding of development and progression in various cancer sub-types. However, the role of lncRNAs in temozolomide (TMZ) resistance in glioblastoma (GBM) remains largely undefined. In this present study, the differential expression of lncRNAs were identified between U87 and U87TR (TMZ-resistant) cells. LncRNA XLOC013218 (XLOC) was drastically upregulated in TMZ-resistant cells and was associated with poor prognosis in glioma. Overexpression of XLOC markedly increased TMZ resistance, promoted proliferation, and inhibited apoptosis in vitro and in vivo. In addition, RNA-seq analysis and gain-of-function or loss-of-function studies revealed that PIK3R2 was the potential target of XLOC. Mechanistically, XLOC recruited Specificity Protein 1 (Sp1) transcription factor and promoted the binding of Sp1 to the promoters of PIK3R2, which elevated the expression of PIK3R2 in both mRNA and protein levels. Finally, PIK3R2-mediated activation of the PI3K/AKT signaling pathway promoted TMZ resistance and cell proliferation, but inhibited cell apoptosis. In conclusion, these data highlight the vital role of XLOC/Sp1/PIK3R2/PI3K/AKT axis in GBM TMZ resistance.
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Project description:PARK2 (PARKIN) is an E3 ubiquitin ligase whose dysfunction has been associated with the progression of Parkinsonism and human malignancies, and its role in cancer remains to be explored. In this study, we investigated its role in glioma. We used microarrays to detail the global programme of gene expression upon PARK2 overexpression in U251 cells U251 cells with PARK2 overexpression or control (GFP) were subjected for RNA extraction and hybridization on Affymetrix microarrays.
2014-10-03 | E-GEOD-61973 | biostudies-arrayexpress
Project description:Temozolomide (TMZ) therapy offers minimal clinical benefits in patients with glioblastoma multiforme (GBM) with high EGFR activity, underscoring the need for effective combination therapy. Here, we show that tonicity-responsive enhancer binding protein (NFAT5) lysine methylation, is a determinant of TMZ response. Mechanistically, EGFR activation induces phosphorylated EZH2 (Ser21) binds and triggers NFAT5 methylation at K668. Methylation prevents NFAT5 cytoplasm interaction with E3 ligase TRAF6, thus blocks TRAF6 induced K63-linked ubiquitination mediated NFAT5 lysosomal degradation and cytosol localization restriction, result in NFAT5 protein stabilization, nuclear accumulation and activation. Methylated NFAT5 leads to the upregulation of MGMT, a transcriptional target of NFAT5, which is responsible for unfavorable TMZ response. Inhibition of NFAT5 K668 methylation improved TMZ efficacy in orthotopic xenografts and PDX models. Notably, NFAT5 K668 methylation levels are elevated in TMZ-refractory specimens and confer poor prognosis. Our findings suggest targeting NFAT5 methylation as an effective therapeutic strategy to improve TMZ response in tumors with EGFR activation.
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Project description:We identified a rare coding variant (p.K420Q) in the complement component 7 (C7) gene affecting the risk of Alzheimer's disease. To investigate the cellular effects of the mutant, we performed RNA-seq in cell line overexpression wilt-type and mutant C7. U251 glioma cells with stable expression of mutant APP (K670N/M671L) (U251-APP cells), which produce Aβ42 under Dox inducing, were used as the model cell. Total RNA of U251-APP cells overexpressing wild type and mutant C7 proteins were subjected to transcriptome sequencing using Illumina Hiseq 4000 platform.
2018-11-22 | GSE101608 | GEO
Project description:G72 is a susceptible gene for schizophrenia. No matter genetic variation or serum levels, G72 has been recognized as a biomarker for schizophrenia. In some reports, G72 genetic variation also related with bipolar disorder. Although G72 has been studied for 15 years, the protein function is still unclear. This study aims for predicting the biological function of G72 and hope to elucidate its biological role. two independent control (U87 cells transfected with empty vector) and two experiements (U87 cells transfected with G72 overexpression plasmid).
2015-12-31 | E-GEOD-67704 | biostudies-arrayexpress
Project description:The discovery of long non-coding RNAs (lncRNAs) has improved the understanding of development and progression in various cancer sub-types. However, the role of lncRNAs in temozolomide (TMZ) resistance in glioblastoma (GBM) remains largely undefined. In this present study, the differential expression of lncRNAs were identified between U87 and U87TR (TMZ-resistant) cells and to find potential therapeutic targets of GBM for improving the survival of patients.
2022-03-30 | GSE199689 | GEO
Project description:Total RNA were extracted from Guanylate Cyclase Soluble Subunit Beta-3 (GUCY1B3) overexpression U87 MG stable cell lines and U87 MG cells. Three RNA samples of each of the two cell lines were used for microarray analysis to compare gene expression profile Guanylate Cyclase Soluble Subunit Beta-3 (GUCY1B3) was cloned into pCDNA3.1D/V5-His-TOPO plasmid (Invitrgen) and then transfected into U87 MG (ATCC HTB-1) cells to generate stable overexpression cells. RNA from the stable cell lines and U87 MG were used for microarray
2016-06-15 | E-GEOD-83344 | biostudies-arrayexpress
Project description:We have employed whole RNA microarray expression profiling as a discovery platform to identify genes regulated by overexpression of miR-145 in U87 glioma cell. Lentivirus containing miR-145 coding sequence was infected to U87 cell to make U87 overexpressing miR-145. We did genome microarray between U87 and U87 overexpressing miR-145.
2011-03-25 | GSE28121 | GEO