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Effect of IDH1 mutation induced by doxycycline on gene expression during VSVΔ51 infection in LN-229-TRE-R132H glioblastoma cells

ABSTRACT: Effect of IDH1 mutation induced by doxycycline on gene expression during VSVΔ51 infection in LN-229-TRE-R132H glioblastoma cells

PROVIDER: PRJNA860394 | ENA |

REPOSITORIES: ENA

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Effect of IDH1 mutation induced by doxycycline on gene expression during VSVΔ51 infection in LN-229-TRE-R132H glioblastoma cells

Project description:To investigate whether IDH1 mutation influence the effects of oncolytic virus VSVΔ51, we transduced doxycycline-inducible IDH1-R132H lentiviruses into LN-229 to establish the LN-229-TRE-R132H cell line. We then performed gene expression profiling analysis using data obtained from RNA-seq of LN-229-TRE-R132H cells infected with or without VSVΔ51 in the presence or absence of IDH1 mutation induced by doxycycline.

2023-09-19 | GSE208634 | GEO

RNA sequencing analysis of LN-229-shControl and LN-229-shMOB2 cells

Project description:RNA sequencing analysis of LN-229-shControl and LN-229-shMOB2 cells

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Identification of JMJD1C target genes in LN-229 glioblastoma cells.

Project description:JMJD1C shows ubiquitous expression and is often downregulated in tumor entities compared to healthy tissues.JMJD1C inhibit growth of the glioblastoma cell line LN-229. Here, JMJD1C knockdown leads to malignant progression in the glioblastoma cell line LN-229.

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Expression data from WIF1 induced LN-229 (GBM cell line)

Project description:Glioblastoma is the most aggressive primary brain tumor in adults and due to the invasive nature it cannot be completely removed. We have recently shown that the WNT inhibitory factor 1 (WIF1), a secreted inhibitor of WNTs, is downregulated in glioblastoma and acts as strong tumor suppressor. In search of a mediator for this function differential gene expression profiles of WIF1-expressing cells were performed. MALAT1, a long non-coding RNA and key positive regulator of invasion, emerged as the top downregulated gene. Indeed, knock-down of MALAT1 reduced migration in glioblastoma cells, without effect on proliferation. LN-229 cells induced with Doxocyclin to express WIF1 were compared to the non-induced control (two biological replicates each)

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Effect of Vortioxetine treatment on gene expression of LN-229 glioblastoma cells over time

Project description:The atypical antidepressant Vortioxetine represents the most effective neuroactive drug with anti-glioblastoma efficacy across glioblastoma patient samples and model systems. To closer examine the temporal dynamics of Vortioxetine, we performed in-depth transcriptomic profiling of LN-229 cells following Vortioxetine treatment. We performed gene expression profiling analysis using data obtained from RNA-seq across 6 different time points during the 24 hours following Vortioxetine treatment.

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Identification of JMJD1C target genes in LN-229 glioblastoma cells.

Project description:Identification of JMJD1C target genes in LN-229 glioblastoma cells.

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Digital RNA with pertUrbation of Genes (DRUG-Seq) of LN-229 glioblastoma cells treated with 20 different drugs at two time points

Project description:DRUG-Seq is a miniatruized and multiplexed RNA-Seq protocol described in Ye et al., 2018 (https://www.nature.com/articles/s41467-018-06500-x) To determine transcriptional changes upon drug perturbation in LN-229 glioblastoma cells, we profiled 20 drug responses across two time-points (6 and 22 hours) by DRUG-Seq

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Gene expression analysis of IDH1 wild type and IDH1 R132H mutated U87 cells

Project description:U87 cells were transduced with IDH1 WT or IDH1 R132H and stable clones were selected.

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DNA methylation alterations and transcriptional gene silencing induced by IDH1 R132H mutation

Project description:This SuperSeries is composed of the following subset Series: GSE31126: DNA methylation alterations and transcriptional gene silencing induced by IDH1 R132H mutation [Affymetrix] GSE31133: DNA methylation alterations and transcriptional gene silencing induced by IDH1 R132H mutation [Illumina] Refer to individual Series

2012-08-12 | E-GEOD-31134 | biostudies-arrayexpress

Idh1-R132H mutation increases murine hematopoietic progenitors and alters epigenetics.

Project description:Mutations in the IDH1 and IDH2 genes encoding isocitrate dehydrogenases are frequent in human glioblastomas1 and cytogenetically normal acute myeloid leukemias (AML)2. These alterations are gain-of-function mutations in that they drive the synthesis of the M-bM-^@M-^\oncometaboliteM-bM-^@M-^] R-2-hydroxyglutarate (2HG)3. It remains unclear how IDH1 and IDH2 mutations modify myeloid cell development and promote leukemogenesis. Here we report the characterization of conditional knock-in mice in which the most common IDH1 mutation, Idh1-R132H, is inserted into the endogenous murine Idh1 locus and is expressed in cells of the hematopoietic (Vav-KI) or more specifically in cells of the myeloid (LysM-KI) lineage. These mutants show increased numbers of early hematopoietic progenitors and develop splenomegaly and anemia with extramedullary hematopoiesis, suggesting a dysfunctional bone marrow niche. Furthermore, LysM-KI cells exhibit both hypermethylated histones and changes to DNA methylation similar to those observed in human IDH1/2-mutant AML. Thus, our study is the first to describe the generation of conditional Idh1-R132H-KI mice. Furthermore, our study is also the first report showing the induction of a leukemic DNA methylation signature in a modeled system and sheds light on the mechanistic links between IDH1 mutation and human AML. DNA methylation profiling in LSK cells from IDH1-R132H knock-in mice vs. control mice

2012-07-22 | E-GEOD-38687 | biostudies-arrayexpress

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