Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Doxorubicin Changes the Spatial Organization of the Genome around Active Promoters

ABSTRACT: To investigate the function of the doxorubicin treatment in differentiation expression of human genes, we performed gene expression profiling analysis using data obtained from RNA-seq of three different conditions: control (DMSO-treatment) and doxorubicin treatment (200 nM and 340 nM).

ORGANISM(S): Homo sapiens

PROVIDER: GSE215321 | GEO | 2023/03/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Doxorubicin Changes the Spatial Organization of the Genome around Active Promoters

Project description:To investigate the function of the TOP2 inhibitors treatment in binding of chromatin architecture factors, we performed ChIP-seq. We used chromatin from RPE1 cells treated with four different conditions: control (DMSO-treatment), doxorubicin treatment (200 nM and 340 nM) and ICRF193 treatment (5uM).

2023-03-31 | GSE215318 | GEO

Doxorubicin Changes the Spatial Organization of the Genome around Active Promoters

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-31 | GSE215325 | GEO

Doxorubicin Changes the Spatial Organization of the Genome around Active Promoters

Project description:To investigate the function of TOP2 on chromatin structure of human cells, we performed Hi-C using chromatin obtained from RPE1 cells.

2023-03-31 | GSE214912 | GEO

Doxorubicin enhances nucleosome turnover around promoters

Project description:We use a metabolic labeling strategy for directly measuring nucleosome turnover to examine the effect of doxorubicin on chromatin dynamics in squamous cell carcinoma cell lines derived from genetically defined mice. We find that doxorubicin enhances nucleosome turnover around gene promoters, and turnover correlates with gene expression level. Keywords: Chromatin affinity-purification on microarray 26 CATCH-IT arrays and 8 expression arrays.

2013-04-19 | E-GEOD-43753 | biostudies-arrayexpress

Doxorubicin enhances nucleosome turnover around promoters

2013-04-19 | GSE43753 | GEO

Doxorubicin enhances nucleosome turnover around promoters.

Project description:Doxorubicin is an anthracycline DNA intercalator that is among the most commonly used anticancer drugs. Doxorubicin causes DNA double-strand breaks in rapidly dividing cells, although whether it also affects general chromatin properties is unknown. Here, we use a metabolic labeling strategy to directly measure nucleosome turnover to examine the effect of doxorubicin on chromatin dynamics in squamous cell carcinoma cell lines derived from genetically defined mice. We find that doxorubicin enhances nucleosome turnover around gene promoters and that turnover correlates with gene expression level. Consistent with a direct action of doxorubicin, enhancement of nucleosome turnover around promoters gradually increases with time of exposure to the drug. Interestingly, enhancement occurs both in wild-type cells and in cells lacking either the p53 tumor suppressor gene or the master regulator of the DNA damage response, ATM, suggesting that doxorubicin action on nucleosome dynamics is independent of the DNA damage checkpoint. In addition, another anthracycline drug, aclarubicin, shows similar effects on enhancing nucleosome turnover around promoters. Our results suggest that anthracycline intercalation promotes nucleosome turnover around promoters by its effect on DNA topology, with possible implications for mechanisms of cell killing during cancer chemotherapy.

| S-EPMC3678987 | biostudies-literature

Sustained Activation of Non-canonical NF-kB Signalling Drives Glycolytic Reprogramming in Doxorubicin-resistant DLBCL

Project description:The transcriptomic profiles of two resistant (HT and OCI-LY3) and two sensitive (SUDHL5 and OCI-LY19) DLBCL cell lines before and after doxorubicin treatment were analysed by RNA-seq. To further investigate the molecular basis underlying the development of doxorubicin resistance, acquired doxorubicin-resistant cells (OCI-LY19R) were generated by periodically treating the parental doxorubicin-sensitive OCI-LY19 cells (OCI-LY19S) with increasing doses of doxorubicin over a prolonged period till its IC50 exceeded 200 nM. RNA-seq analysis was then performed using OCI-LY19R and OCI-LY19S cell lines to examine the transcriptomic changes following acquisition of doxorubicin resistance.

2022-12-01 | GSE215900 | GEO

Gene expression profile in response to doxorubicin-rapamycin combined treatment of HER-2 overexpressing human mammary epithelial cell lines

Project description:HER-2 positive breast cancers frequently sustain elevated AKT/mammalian target rapamycin (mTOR) signaling which has been associated with resistance to doxorubicin treatment in the clinic. In our study we investigated if the mTOR inhibitor rapamycin increased the sensitivity to doxorubicin therapy in HB4a, a luminal normal mammary cell line; C5.2, a transformed cell derived from HB4a transfected with HER-2 and SKBR3 that exhibits HER-2 amplification. Flow cytometry analysis showed that the combination treatment for 24 hours with rapamycin 20nM and doxorubicin caused accumulation of HB4a and C5.2 cells in S-G2/M. Otherwise in SKBR3 cells, we observed a relative depletion of cells in S-G2/M and concomitant accumulation in G0/G1 of 10% of the cells. The analysis of IC50 of doxorubicin alone and in combination with rapamycin indicated that the sensitivity was increased 2.37 fold in HB4a, 2.46 in C5.2 and 1.87 in SKBR3, suggesting that rapamycin might have enhanced the effects of doxorubicin. Changes in gene expression resulting from co-treatment demonstrated that functional groups of genes with roles in cell cycle, proliferation, apoptosis regulation were represented in the 3 cells analysed. Other biological functions were exclusively associated with each cell suggesting that the inhibition of mTOR activation induced by HER-2 is complex and depends on the cellular context. Five independent experiments were performed for each treatment conditions: HB4a, C5.2 and SKBR3 cell lines were treated with vehicle (DRC), 20 nM of RAPAMYCIN alone (R) and 30 nM of DOXORUBICIN alone (D). The combined treatment consisted of 20 nM of RAPAMYCIN associated with 30 nM DOXORUBICIN of (DR). Total RNA extraction and hybridization on Affymetrix microarrays.

2011-01-13 | E-GEOD-26599 | biostudies-arrayexpress

Bulk RNA-seq of Normal and Doxorubicin-Induced Senescent HCA2 cells

Project description:Purpose: Use RNA-seq strategy to characterize the PD-L1 correlated genes in sorted PD-L1 negative and positive doxorubicin-induced senescent and normal human foreskin fibroblasts HCA2 cells to identify the upstream transcriptional network for regulating heterogeneous PD-L1 expression in senescent cells. Methods: Early passaged normal HCA2 cells and senescent HCA2 cells induced by 24 hours of 100 nM doxorubicin treatment were utilized for the preparation of bulk RNA-seq libraries. Among the senescent cells, PD-L1 positive and negative cells were separated by FACSorting.

2022-08-27 | GSE198396 | GEO

Detoxifying doxorubicin

Project description:The anthracycline doxorubicin is a highly effective anti-cancer drug associated with severe side effects, including secondary tumors and cardiotoxicity. Doxorubicin induces DNA damage through double-strand breaks (DSBs) and epigenetic or chromatin damage through histone eviction. We examined whether separation of these activities can help to detoxify doxorubicin, while maintaining its chemotherapeutic efficacy. We show that anthracycline variants harboring the histone eviction activity alone remain potent anti-cancer drugs, while greatly alleviating cardiotoxicity and secondary tumor formation. We thus demonstrate that treatment-limited side effects of doxorubicin can be synthesized away, yielding effective chemotherapeutics towards improved and prolonged treatment responses and higher patient quality of life.

2019-09-01 | GSE108179 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data