Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq analysis of AKTi MK2206 resistant BT474 and T47D cells

ABSTRACT: RNA-seq analysis of AKTi MK2206 resistant BT474 and T47D cells

PROVIDER: PRJNA484709 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7647424_1.fastq.gz	Fastqsanger.gz
	SRR7647424_2.fastq.gz	Fastqsanger.gz
	SRR7647425_1.fastq.gz	Fastqsanger.gz
	SRR7647425_2.fastq.gz	Fastqsanger.gz
	SRR7647427_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

RNA-seq analysis of AKTi MK2206 resistant BT474 and T47D cells

Project description:BRD4 assembles transcriptional machinery at gene super-enhancer regions and governs the expression of genes that are critical for cancer progression. However, it remains unclear whether BRD4-mediated gene transcription is required for tumor cells to develop drug resistance. Our data show that prolonged treatment of luminal breast cancer cells with AKT inhibitors induces FOXO3a de-phosphorylation, nuclear translocation, and disrupts its association with SIRT6, eventually leading to FOXO3a acetylation as well as BRD4 recognition. Acetylated FOXO3a recognizes the BD2 domain of BRD4, recruits the BRD4/RNAPII complex to the CDK6 gene promoter and induces its transcription. Pharmacological inhibition of either BRD4/FOXO3a association or CDK6 significantly overcomes the resistance of luminal breast cancer cells to AKT inhibitors in vitro and in vivo. Our study reports the involvement of BRD4/FOXO3a/CDK6 axis in AKTi resistance and provides potential therapeutic strategies for treating resistant breast cancer.

2019-02-21 | GSE118148 | GEO

Messenger RNA expression after MK2206/DMSO treatment of T47D cells

Project description:We performed RNA-seq in T47D cells after 24 hour treatment with the AKT inhibitor MK2206 or DMSO. We show that a group of transcripts is differentailly expressed after AKT inhibition.

2016-06-14 | GSE80591 | GEO

Genome-wide H3K4me3 after MK2206/DMSO treatment of T47D cells

Project description:We perfomed ChIP-seq using H3K4me3 antibodies in T47D cells after 24 hour treatment with the AKT inhibitor MK2206 or DMSO. We demonstrate that at a selected group of loci H3K4me3 is affected by AKT inhibition.

2016-06-14 | GSE80592 | GEO

Genome-wide KDM5A occupancy after MK2206/DMSO treatment of T47D cells

Project description:We perfomed ChIP-seq using KDM5A antibodies in T47D cells after 24 hour treatment with the AKT inhibitor MK2206 or DMSO. We show that the cistrome of the H3K4 demethylase KDM5A is affected by AKT inhibition.

2016-06-14 | GSE80593 | GEO

Messenger RNA expression after MK2206/DMSO treatment of T47D cells

2016-06-14 | E-GEOD-80591 | biostudies-arrayexpress

Genome-wide H3K4me3 after MK2206/DMSO treatment of T47D cells

2016-06-14 | E-GEOD-80592 | biostudies-arrayexpress

Genome-wide KDM5A occupancy after MK2206/DMSO treatment of T47D cells

2016-06-14 | E-GEOD-80593 | biostudies-arrayexpress

RNA sequencing of BT474 cells treated with trastuzumab or trastuzumab + pertuzumab and BT474-derived cells resistant to trastuzumab or trastuzumab + pertuzumab

Project description:We sequenced untreated BT474 cells, BT474 cells treated for three days with trastuzumab or trastuzumab + pertuzumab, as well as two BT474-derived trastuzumab-resistant pools and two BT474-derived trastuzumab + pertuzumab resistant pools. Resistant pools were generated by culturing BT474 cells in gradually increasing doses of trastuzumab and trastuzumab + pertuzumab over the course of several months and continually maintained in drug.

2020-01-26 | GSE121105 | GEO

BT474 and BT474-J4 microarray data

Project description:These data provide scientific information to understand the mechanism of action of lapatinib resistance in HER2-positive patients and to test the combination of HER2-targeted agents and GSK1363089 (foretinib) in the clinic by using an acquired lapatinib-resistant cell line. Cell lines (BT474, an HER2-positive and lapatinib-sensitive cell line; BT474-J4, an acquired lapatinib-resistant cell line) were treated with lapatinib alone (1uM), foretinib (GSK1363089) alone (0.1 uM), a combination of lapatinib (1 uM) and foretinib (0.1 uM), or DMSO control for 24 hours. Triplicates were performed.

2011-09-19 | E-GEOD-16179 | biostudies-arrayexpress

Differential expression levels of mRNAs in tamoxifen-sensitive T47D versus tamoxifen-resistant T47D (T47DR) human breast cancer cells

Project description:Tamoxifen is the most widely used antiestrogen in patients with estrogen receptor (ER) positive breast cancer . However, less than half of patients benefit from tamoxifen treatment and 30-50% acquire resistance and the disease progresses. Resistance to tamoxifen is a serious problem in breast cancer therapy and major efforts are underway to find out underlying mechanisms. To find out the differential expression levels of mRNAs in tamoxifen-sensitive T47D versus tamoxifen-resistant T47D (T47DR) human breast cancer cells, T47DR (tamoxifen-resistant) cell line was established from T47D cells after the following continuous exposure to 1 μmol/L 4-Hydroxytamoxifen (H7904, Sigma, USA) for more than 6 months.Thousands of significantly different mRNA expression levels were found and analysed. Our study provides a reference data for the study of tamoxifen resistance .

2020-06-01 | GSE129544 | 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