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Transcriptomic analysis of LN229 cell treated by unit of bortezomib and panobinostat

ABSTRACT: We report the application of unit of bortezomib and panobinostat on LN229 cell , and further explored the mechanism of drugs on GBM cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE206984 | GEO | 2022/06/30

REPOSITORIES: GEO

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Transcriptomic analysis of LN229 cell treated by unit of bortezomib and panobinostat

Project description:Transcriptomic analysis of LN229 cell treated by unit of bortezomib and panobinostat

| PRJNA853204 | ENA

Effect of panobinostat, givinostat and ruxolitinib treatment in the anti-GBM mouse model of crescentic glomerulonephritis.

Project description:We demonstrated that in anti-glomerular basement membrane (anti-GBM) glomerulonephritis, crescents derived from clonal amplification of an immature subset of parietal epithelial cells (PECs) and that following treatment of mice with 3 different drugs currently used in haematological stem cell disorders (panobinostat, givinostat and ruxolitinib), only panobinostat exerted beneficial effect. To establish the mechanism of action of panobinostat, we generated single-cell RNA sequencing (scRNAseq) datasets of kidney cells obtained from control mice with anti-GBM glomerulonephritis and of mice treated with the three drugs. The analysis demonstrated that the drugs exerted similar effects on clusters of cells of the immune system, suggesting that all the three drugs elicit similar anti-inflammatory and immunosuppressive properties.

2022-09-24 | GSE195784 | GEO

Expression data of LN229 cells treated with 23 Pa compressive solid stress (CSS) or no CSS

Project description:Glioblastoma ( GBM) is an astrocytic brain tumor with median survival times of < 15 months, primarily as a result of high infiltrative potential and development of resistance to therapy (i.e., surgical resection, chemoradiotherapy). A prominent feature of the GBM microenvironment is compressive solid stress (CSS) caused by uninhibited tumor growth within the confined skull. We used microarrays to explore the gene expression of LN229 cells treated with 23 Pa CSS as compared to no CSS. The purpose is to detect the up-regulated genes induced by CSS.

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RNA-seq analysis of gene expression profile in PTEN WT and KO LN229 glioblastoma multiforme (GBM) Xenograft tumor Transcriptomes

Project description:The goal of this study is to compare gene expression profiles of PTEN WT and KO GBM cells when they are growing in vivo. Isogenic PTEN WT or KO LN229 GBM cells were subcutaneously implanted into Balb/c nude mice (two in each group) to form tumor. At the 30th day tumors were harvested and total RNA was isolated. RNA-seq analysis was performed to examine the differential express pattern of the two type of xenografts.

2019-09-04 | GSE136738 | GEO

Differential gene expression in neuroblastoma cells after treatment with vehicle control, JQ1, panobinostat, or combination of JQ1 and panobinostat

Project description:The bromodomain inhibitor JQ1 and the histone deacetylase inhibitor panobinostat induce synergistic anticancer effects We analyzed whether JQ1 and panobinostat synergistically modulate gene expression Neuroblastoma SK-N-BE(2) cells were treated with vehicle control, 1 microM JQ1, 10 nM panobinostat, or combination of JQ1 and panobinostat for 6 hours, and subjected to differential gene expression studies with Affymetrix microarrays.

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Plasma Mouse LC-MSMS - Bortezomib administered prior to temozolomide depletes MGMT, chemosensitizes glioblastoma with unmethylated MGMT promoter and prolongs animal survival

Project description:Patients diagnosed with glioblastoma (GBM) with sustained synthesis of the DNA repair enzyme, O6-methyl guanine DNA methytransferase (MGMT), are rendered resistant to Temozolomide (TMZ) chemotherapy. Here, we hypothesized that pretreatment with the proteasome inhibitor Bortezomib (BTZ, Velcade) might sensitize these GBM to TMZ by depleting MGMT.

2019-08-20 | PXD007193 | Pride

A Subset of Genes Can Distinguish between Bortezomib Responsive Versus Bortezomib Resistant Myeloma

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NCI-H1688 cells treated with natural compounds(sanguinarine chloride, cepharanthine and evodiamine), or (+)-JQ-1, or panobinostat, or sanguinarine chloride in combination with panobinostat or (+)-JQ-1.

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2021-08-31 | GSE182821 | GEO

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Project description:Purpose: We applied RNA sequencing technology for high-throughput analysis of transcriptional changes within human MM cell lines JJN3 and U266 due to individual and combination drug treatment. Methods: JJN3 and U266 cells were treated with pan-HDACi panbobinostat, DNMTi 5-Azacytidine, panobinostat+5-Azacytidine or NMP for 4h or 24h in triplicate and transcriptional changes assessed by RNAseq using Illumina HiSeq platform. Specifically, JJN3 cells were treated with 10nM panobinostat, 2.5µM 5-Azacytidine, panobinostat+5-Azacytidine (at given doses), or 10mM NMP. U266 cells were treated with 10nM panobinostat, 10µM 5-Azacytidine, panobinostat+5-Azacytidine (at given doses), or 10mM NMP. Results: We report unique and overlapping transcriptional signatures that lead to the induction of apoptosis in human MM cell lines in a cell-specific manner due to individual or combination treatments. Conclusions: A detailed analysis of differential transcriptional events in human MM cell lines due to HDACi, DNMTi, HDACi+DNMTi and NMP appear to define the molecular events leading to apoptosis and drug mechanism of action. We tested triplicate experiments at 4h and 24hr time points in JJN3 and U266 cell lines against vehicle control treated cells.

2014-04-09 | E-GEOD-56623 | biostudies-arrayexpress

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2016-07-31 | GSE71435 | GEO

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