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

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

PROVIDER: PRJNA853204 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19859500_1.fastq.gz	Fastqsanger.gz
	SRR19859500_2.fastq.gz	Fastqsanger.gz
	SRR19859493_1.fastq.gz	Fastqsanger.gz
	SRR19859493_2.fastq.gz	Fastqsanger.gz
	SRR19859494_1.fastq.gz	Fastqsanger.gz

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

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

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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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Transcriptomic alterations upon HSP90 inhibition in human LN229 and T98 glioblastoma cells in vitro

Project description:Purpose: Characterization of transcriptomic alterations upon HPS90 inhibition in human LN229 and T98G glioblastoma cells in vitro. Methods: LN229 and T98G glioblastoma cells were treated with 10 nM of the HSP90 inhibitor NW457 or the vehicle control for 24 h, and total RNA was subjected to 3' RNA sequencing. Results: Distinct transcriptomic alterations were observed, dominated by a transcriptional upregulation of the heat shock response. Conclusion: HSP90 inhibition resulted in distinct transcriptomic alterations and a clear upregulation of the heat shock response.

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Bulk RNAseq of A375 cells treated with Panobinostat

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ChIP-Seq of TRIB3 and ATF4 in HepG2 cells treated with bortezomib

Project description:The proteasome is an appealing anti-cancer drug target and the proteasome inhibitor bortezomib has been approved for the treatment of certain types of malignancies. However, the molecular mechanisms underlying cancer cell resistance to bortezomib remain poorly understood. The pseudokinase TRIB3, an inhibitor of ATF4, is expressed at a high basal level in hepatoma cells and is strongly upregulated in response to bortezomib. To map genome-wide chromatin binding loci of TRIB3 protein, we fused a Flag tag to endogenous TRIB3 in HepG2 cells and performed ChIP-Seq. The results demonstrate that TRIB3 predominantly colocalizes with ATF4 on chromatin and the proteins reside in genomic regions containing the C/EBP-ATF motif. Bortezomib treatment leads to a robust enrichment of TRIB3 binding near genes induced by bortezomib and involved in the ER stress response and cell death. Disruption of TRIB3 increases C/EBP-ATF-driven transcription, augments ER stress and cell death in cells exposed to bortezomib, while TRIB3 overexpression enhances the cell survival. Thus, TRIB3, colocalizing with ATF4 and limiting its transcriptional activity, functions as a factor increasing resistance to bortezomib, while pharmacological over-activation of eIF2alpha-ATF4 can overcome the endogenous restraint mechanisms and sensitize cells to bortezomib.

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Project description:Panobinostat is a potent pan-deacetylase inhibitor that affects the growth and survival of multiple myeloma (MM) cells through alteration of epigenetic mechanisms and protein metabolism. Panobinostat plus bortezomib and dexamethasone (PAN-BTZ-Dex) led to a significant increase in progression-free survival (PFS) vs placebo plus bortezomib and dexamethasone (Pbo-BTZ-Dex) in patients with relapsed or relapsed and refractory MM in the phase 3 PANORAMA 1 trial. This subgroup analysis evaluated outcomes in patients in the PANORAMA 1 trial based on prior treatment: a prior immunomodulatory drug (IMiD; n = 485), prior bortezomib plus an IMiD (n = 193), and ≥2 prior regimens including bortezomib and an IMiD (n = 147). Median PFS with PAN-BTZ-Dex vs Pbo-BTZ-Dex across subgroups was as follows: prior IMiD (12.3 vs 7.4 months; hazard ratio [HR], 0.54; 95% confidence interval [CI], 0.43-0.68), prior bortezomib plus IMiD (10.6 vs 5.8 months; HR, 0.52; 95% CI, 0.36-0.76), and ≥2 prior regimens including bortezomib and an IMiD (12.5 vs 4.7 months; HR, 0.47; 95% CI, 0.31-0.72). Common grade 3/4 adverse events and laboratory abnormalities in patients who received PAN-BTZ-Dex across the prior treatment groups included thrombocytopenia, lymphopenia, neutropenia, diarrhea, and asthenia/fatigue. Incidence of on-treatment deaths among patients who received prior bortezomib and an IMiD (regardless of number of prior regimens) was similar between treatment arms. This analysis demonstrated a clear PFS benefit of 7.8 months with PAN-BTZ-Dex among patients who received ≥2 prior regimens including bortezomib and an IMiD, a population with limited treatment options and poorer prognosis. This trial was registered at www.clinicaltrials.gov as #NCT01023308.

| S-EPMC4760132 | biostudies-literature

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