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Functionally-instructed modifiers of response to ATR inhibition in experimental glioma

ABSTRACT: We investigated the influence of ATR inhibition by AZD6738 treatment in LN229 and LNZ308 glioma cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE229614 | GEO | 2024/03/22

REPOSITORIES: GEO

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Functionally-instructed modifiers of response to ATR inhibition in experimental glioma

Project description:Functionally-instructed modifiers of response to ATR inhibition in experimental glioma

| PRJNA955169 | ENA

Functionally-instructed modifiers of response to ATR inhibition in experimental glioma.

Project description:BackgroundThe DNA damage response (DDR) is a physiological network preventing malignant transformation, e.g. by halting cell cycle progression upon DNA damage detection and promoting DNA repair. Glioblastoma are incurable primary tumors of the nervous system and DDR dysregulation contributes to acquired treatment resistance. Therefore, DDR targeting is a promising therapeutic anti-glioma strategy. Here, we investigated Ataxia telangiectasia and Rad3 related (ATR) inhibition (ATRi) and functionally-instructed combination therapies involving ATRi in experimental glioma.MethodsWe used acute cytotoxicity to identify treatment efficacy as well as RNAseq and DigiWest protein profiling to characterize ATRi-induced modulations within the molecular network in glioma cells. Genome-wide CRISPR/Cas9 functional genomic screens and subsequent validation with functionally-instructed compounds and selected shRNA-based silencing were employed to discover and investigate molecular targets modifying response to ATRi in glioma cell lines in vitro, in primary cultures ex vivo and in zebrafish and murine models in vivo.ResultsATRi monotherapy displays anti-glioma efficacy in vitro and ex vivo and modulates the molecular network. We discovered molecular targets by genome-wide CRISPR/Cas9 loss-of-function and activation screens that enhance therapeutic ATRi effects. We validated selected druggable targets by a customized drug library and functional assays in vitro, ex vivo and in vivo.ConclusionIn conclusion, our study leads to the identification of novel combination therapies involving ATRi that could inform future preclinical studies and early phase clinical trials.

| S-EPMC10935927 | biostudies-literature

Diosmin inhibits glioma growth through inhibition of autophagic flux

Project description:RNA microarray was performed from glioma cell LN229 and GBM8401 that were treated with Diosmin (160 nM) for 48hr in comparison to DMSO vehicle control.

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Genes regulated by Sox2 in glioma cancer cell line

Project description:Knockdown of Sox2 in LN229 gliomal cancer cells decrease their growth rates in vitro. We used microarrays to detail the global programme of gene expression in Sox2 Knockdown LN229 cells compared with mock knockdown LN229 cells Sox2 knockdown LN229 cells and and mock knockdown LN229 cells were cultured in DMEM cell culture media for RNA extraction and hybridization on Applied Biosystems Human Genome Survey Microarrays . We sought to obtain the genes regulated by Sox2 in glioma cell line.

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Oligoadenylate synthetase-like (OASL) aggravated newcastle disease virus (NDV)-induced necroptosis in glioma cells

Project description:Newcastle disease virus (NDV) has emerged as an oncolytic agent in several cancers. Previous study has shown that NDV exerts cytolytic activity in glioma, however, the underlying mechanism has not been fully uncovered. Here the cytolytic activity of NDV in glioma and the associated mechanisms have been demonstrated. Infection with NDV inhibits cell proliferation and promotes cell apoptosis in LN229 cells. Further investigation showed that cytoplasmic organelle damage and cytoplasmic vacuolation were observed in LN229 cells after NDV infection. JC-1 staining assay proved that NDV caused cell apoptosis of LN229 cells by inducing mitochondrial dysfunction. We next speculated that NDV caused LN229 cells death through inducing necroptosis, but not ferroptosis, since the Fe2+ level did not alter after NDV infection. Furthermore, the NDV-caused cell death in LN229 cells was blocked by necroptosis inhibitor Nec1. Besides, RNA-seq analysis identified the different expression genes in NDV-infected LN229 cells. OASL, an antiviral gene, has been found to be directly induced by NDV infection. We also found that knockdown of OASL enhanced NDV infection-induced LN229 cells necroptosis. In summary, two aspects about cytolytic activity of NDV in glioma have been demonstrated. NDV presented cytolytic activity in glioma cells through inducing necroptosis. Additionally, targeting OASL may provide new strategy for enhancing necroptosis of glioma cells after NDV infection.

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miR-139-5p induced gene expression alteration in glioma cells

Project description:To evaluate gene expression alteration following miR-139-5p transfection in glioma cells. We find a significant downregulation of two transcriptional factors, E2F3 and HoxA9. Total RNA were extracted from U87, LN229 and U251 glioma cells transfected with miR-139-5p or miRNA negative control.

2013-03-01 | E-GEOD-44728 | biostudies-arrayexpress

Momordicine I Suppresses Glioma Growth by Promoting Apoptosis and Impairing Mitochondrial Oxidative Phosphorylation

Project description:RNA microarray was performed from glioma cell LN229 and GBM8401 that were treated with Momordicine (10 microM) for 48hr in comparison to DMSO vehicle control

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The effect of ATR inhibition on the replication timing program

Project description:As a part of the project looking into the role of ATR in regulating replication initiation, we report the replication timing analysis of the U2OS cells treated with ATR kinase inhibitor AZD6738

2019-07-26 | GSE131018 | GEO

Genome-wide fork-collapse sites in MEFs from ATR inhibition

Project description:Transient obstruction of DNA polymerase progression activates the ATR checkpoint kinase, which suppresses fork breakage, strand resection, and RPA accumulation. Herein, we use RPA ChIP-Seq to identify replication-problematic loci (RPLs) across the mammalian genome from ATR inhibition.

2018-10-04 | GSE100790 | GEO

The effect of ATR inhibition on the replication timing program

Project description:as a part of the project looking into the role of ATR in regulating replication initiation and to investigate the rapid replication of CD8+ T cells, we report the replication timing analysis of murine CD8+ T cells and fibroblasts treated with ATR kinase inhibitor AZD6738

2022-05-01 | GSE183412 | GEO

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