Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

AS1842856 treatment in BT549 cells

ABSTRACT: Basal-like breast cancer (BBC) is a poor prognosis cancer that lacks effective targeted therapy. Recently our group and others found that forkhead box transcription factor FOXO1 promotes stem gene expression in BBC and GBM cell lines. Given the critical role of cancer stem cells in promoting cancer progression, we examined the impact of FOXO1 inhibition with AS1842856 on BBC cells. We treated BT549 cells with 200nM AS1842856 for 48 hours and found that FOXO1 inhibition induced a set of WNT Pathway genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE179856 | GEO | 2023/11/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

AS1842856 treatment in BT549 cells

Project description:AS1842856 treatment in BT549 cells

| PRJNA745342 | ENA

Transcriptome analysis of BT549 cells overexpressing SNHG15

Project description:LncRNA SNHG15 is an oncogenic lncRNA in a variety of cancers including breast cancer, lung cancer, and hepatocellular carcinoma. To screen genes regulated by SNHG15, we performed RNA-seq with stable SNHG15-overexpression BT549 cells, using BT549-pcIP2 as control.

2023-06-08 | GSE220492 | GEO

Gene expression profiling of MDA231, BT549, and SUM159PT cells after selumetinib treatment or DUSP4 siRNA knockdown

Project description:MDA231, BT549, and SUM159PT basal-like breast cancer cell lines were transfected with non-targeting siRNA (siCONTROL), siRNA targeting DUSP4 (siDUSP4), or siCONTROL + 4 or 24 hr of 1uM selumetinib. Cells were harvested at 96 hr post-siRNA transfection. Data were Log2 RMA normalized. We sought to identify changes in gene expression after MEK inhibition, or after loss of DUSP4 function in breast cancer cell lines.

2013-09-03 | E-GEOD-41816 | biostudies-arrayexpress

CDK7-dependent Transcriptional Addition in Basal-like Breast Cancer

Project description:Basal-like breast cancer (BBC) is a highly aggressive form of breast cancer that exhibits extremely high levels of genetic complexity and yet a relatively uniform transcriptional program. We postulate that BBC might be highly dependent on uninterrupted transcription of a key set of genes within this gene expression program and might therefore be exceptionally sensitive to inhibitors of transcription. Utilizing a novel kinase inhibitor and CRISPR/Cas9-mediated gene editing, we show here that basal but not luminal breast cancer cells are exceptionally dependent on CDK7, a transcriptional cyclin-dependent kinase. BBC cells are unique in their dependence on this transcriptional CDK and suffer apoptotic cell death upon CDK7 inhibition. An “Achilles cluster” of BBC-specific genes are extremely sensitive to CDK7 inhibition and frequently associated with super-enhancers. We conclude that CDK7 mediates transcriptional addiction to a vital cluster of genes in BBC and CDK7 inhibition may be useful therapy for this challenging cancer. ChIP-Seq for H3K27ac in basal-like breast cancer and luminal-like breast cancer cell lines

2015-01-23 | E-GEOD-65201 | biostudies-arrayexpress

Transcriptomics modification consecutive to AS1842856 treatment in primary T lymphocytes

Project description:We have observed that the FOXO1 inhibitor AS1842856 induces a significant increase of both the bioenergetics and transcriptional activity of human T cells, together with a significant increase in their size, without any cell division. These modifications are accompanied by a decrease of p27 expression, contrasting with an increase of CDK2 cellular levels and by the phosphorylation of Rb and SAMHD1 proteins. As these changes are known to be characteristic of cells undergoing a G0 to G1 progression. To get an overall view of these changes in T-cell metabolism, we performed gene expression microarray analysis of PBT cultured during 7 days in the presence or not of AS1842856. We conclude that inhibition of FOXO1 by AS1842856 is sufficient to induce a profound reprogramming of human T lymphocytes, regulating their exit from quiescence.

2019-03-08 | GSE125328 | GEO

CDK7-dependent Transcriptional Addition in Basal-like Breast Cancer (ChIP-Seq)

2015-01-23 | GSE65201 | GEO

BT549 cells with control or NFIL3 shRNA treatment

Project description:Transcriptional profiling with samples from BT549 cells that were infected with control or NFIL3 shRNA

2012-09-02 | GSE31425 | GEO

miR-200c induction in BT549 TNBC cells

Project description:We performed microarray analysis on BT549 cells that express miR-200c in a doxycycline (dox)-inducible manner from the miR-200c-TripZ system.

2017-12-20 | GSE108271 | GEO

aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA binding ability

Project description:Strict regulation of proliferation is vital for development, whereas unregulated cell proliferation is a fundamental characteristic of cancer. The polarity protein atypical protein kinase C lambda/iota (aPKC lambda) is associated with cell proliferation through unknown mechanisms. In endothelial cells, suppression of aPKC lambda impairs proliferation despite hyperactivated mitogenic signaling. Here we show that aPKC lambda phosphorylates the DNA binding domain of forkhead box O1 (FoxO1) transcription factor, a gatekeeper of endothelial growth. Although mitogenic signaling excludes FoxO1 from the nucleus, consequently increasing c-Myc abundance and proliferation, aPKC lambda controls c-Myc expression via FoxO1/miR-34c signaling without affecting its localization. We find this pathway is strongly activated in the malignant vascular sarcoma, angiosarcoma, and aPKC inhibition reduces c-Myc expression and proliferation of angiosarcoma cells. Moreover, FoxO1 phosphorylation at Ser218 and aPKC expression correlates with poor patient prognosis. Our findings may provide a new therapeutic strategy for treatment of malignant cancers, like angiosarcoma.

2019-11-12 | PXD011595 | Pride

BT549 cells with control or NFIL3 shRNA treatment

Project description:Transcriptional profiling with samples from BT549 cells that were infected with control or NFIL3 shRNA Two condition experiment: control (scr) shRNA (two replicates) and NFIL3 shRNA (two replicates)

2012-09-02 | E-GEOD-31425 | biostudies-arrayexpress

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