Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Leukemic cell lines expression profile of OTX015 compared to JQ1 and DMSO controls

ABSTRACT: Gene signature determination of the effect of a new bromodomain inhibitor among a representative set of leukemic cell lines

ORGANISM(S): Homo sapiens

PROVIDER: GSE70263 | GEO | 2015/06/25

SECONDARY ACCESSION(S): PRJNA288129

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Leukemic cell lines expression profile of OTX015 compared to JQ1 and DMSO controls

Project description:Gene signature determination of the effect of a new bromodomain inhibitor among a representative set of leukemic cell lines OTX015 vs. DMSO and JQ1 vs. DMSO

2015-06-25 | E-GEOD-70263 | biostudies-arrayexpress

Multiple myeloma cell lines expression profile of OTX015-treated cells compared to DMSO controls

Project description:Several studies demonstrate that the bromodomain inhibitor OTX015 has preclinical antitumor activity in a variety of solid tumors and hematologic cancers. However, translation of these data to molecules suitable for clinical development has not yet to be accomplished in multiple myeloma (MM). Here, we identified genes and biologic processes that underpin the antimyeloma activity of OTX015 with global transcriptomics. OTX015 exerted strong antiproliferative effect and induced cell cycle arrest in vitro. Gene expression profiling showed that OTX015 targeted NF-κB, EGFR, cell cycle regulation, cancer proliferation signaling pathway. Gene expression signatures associated with different sensitivity to OTX015 were also identified. The data also showed that oral administration of OTX015 displayed significant antitumor activity in mice model of disseminated human myeloma. In addition, our study provided the first evidence and rationale that OTX015 could promoted osteoblast differentiation of mesenchymal stem cells (MSCs) and inhibited osteoclast formation and resorption in vivo experiments. Herein we expanded the mechanistic understanding of BET inhibitors OTX015 in MM. Our preclinical studies provided a strong rationale for extending the clinical testing of the novel antimyeloma agent OTX015 and revealed insights into biologic pathways required for myeloma cell proliferation.

2019-03-08 | GSE111422 | GEO

Targeting of SMARCA4 bromodomain selectively inhibits leukemic cell proliferation

Project description:Targeting of SMARCA4 bromodomain selectively inhibits leukemic cell proliferation

| PRJNA281224 | ENA

Leukemic hematopoiesis

Project description:Leukemic hematopoiesis

| PRJNA881262 | ENA

Multiple myeloma cell lines expression profile of OTX015-treated cells compared to DMSO controls

Project description:Multiple myeloma cell lines expression profile of OTX015-treated cells compared to DMSO controls

| PRJNA436970 | ENA

Biological Effects of BET Inhibition by OTX015 (MK-8628) and JQ1 in NPM1-Mutated (NPM1c) Acute Myeloid Leukemia (AML).

Project description: Not available

| S-EPMC8615962 | biostudies-literature

Differential gene expression in neuroblastoma cells after treatment with JQ1, nanaomycin, or combination of JQ1 and nanaomycin

Project description:BET bromodomain inhibitors are emerging as very promising novel anticancer agents. Combination of BET bromodomain inhibitor JQ1 and quinone-containing compound nanaomycin exerts synergistic anticancer effect in neuroblastoma We analysed whether a treatment with BET bromodomain inhibitor JQ1, and quinone-containing compound Nanaomycin synergistically modulate gene expression

2016-12-31 | GSE76066 | GEO

Transcriptional profiling of triple-negative breast cancer cell lines treated with OTX015

Project description:In order to determine the impact on transcription of the novel bromodomain inhibitor OTX015, we treated two triple-negative breast cancer cell lines (MDA-MB-231 and MDA-MB-468) treated with the compound at 24 hours.

2018-01-16 | E-MTAB-3862 | biostudies-arrayexpress

A Generalized Strategy to Kill Leukemic Cells by Targeting the Regulatory Systems Governing Mitochondrial Membrane Potential

Project description:Targeting mitochondria emerges as a promising anti-leukemia strategy, yet selective mitochondrial disruption remains challenging. Here, we identified elevated mitochondrial membrane potential (MMP) as a hallmark of leukemic transformation and chemotherapy-resistant cells, prompting screening for MMP-targeting agents. Alexidine, an MMP-depleting compound, demonstrated potent anti-leukemic activity with low toxicity. Mechanistically, Alexidine binds unsaturated cardiolipin to destabilize the inner membrane localization of mitochondrial ribosome, suppressing cardiolipin-dependent mitochondrial translation, a process validated as an independent prognostic marker in leukemia. Unlike chemotherapy, Alexidine eradicates baseline MMP and MMP heterogeneity within leukemic populations, a functional signature linked to stemness and chemoresistance. Intriguingly, this heterogeneity originates not from cardiolipin-mediated translation but from asparagine-driven mitochondrial protein synthesis, which leukemia cells selectively activate to bypass chemotherapy. Critically, pharmacological asparagine depletion synergistically enhances chemosensitivity by disrupting this resistance pathway. Our findings establish that MMP regulation through cardiolipin-maintained homeostasis and asparagine-fueled adaptation represents therapeutic vulnerabilities, advocating co-targeting strategies to overcome resistance.

2025-07-11 | MTBLS12596 | MetaboLights

FOXO-inhibited iPSC-derived cardiomyocytes compared against DMSO vehicle controls.

Project description:Human induced pluripotent stem cell (iPSC)-derived cardiomyocytes cultured in 3-dimensional suspension culture were treated with AS1842856 FOXO-inhibitor (n=3 independent wells) or DMSO vehicle control (n=3 independent wells). Total RNA was isolated from each well and utilized for RNA sequencing.

2024-08-09 | GSE252627 | 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