Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of breast cancer cell lines post ligand treatment I

ABSTRACT: Goal: study the impact of estrogen receptor ligands on gene expression in HR+ breast cancer cells Methods: RNA sequencing Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), promotes transcriptional activation of ER and mimics the transcriptional effect of natural ligand E2 for a subset of ER target genes, consistently across the seven breast cell lines (MCF-7, HCC1500, MDA-MB-330, EFM-19, T-47D, BT-474, and CAMA-1). Selective ER degraders (SERD) fulvestrant and GDC-0927 on the other hand do not induce, or induce very weakly the expression of ER target genes. The effect of GDC-0810 depends on the cellular context.

ORGANISM(S): Homo sapiens

PROVIDER: GSE117942 | GEO | 2019/07/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq of breast cancer cell lines post ligand treatment II

Project description:Goal: study the impact of estrogen receptor ligands on gene expression in HR+ breast cancer cells Methods: RNA sequencing Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), promotes transcriptional activation of ER and mimics the transcriptional effect of natural ligand E2 for a subset of ER target genes, consistently across the seven breast cell lines (MDA-MB-134 VI, MDA-MB-330, EFM-19, T-47D, and BT-474). Selective ER degraders (SERD) fulvestrant and GDC-0927 on the other hand do not induce, or induce very weakly the expression of ER target genes. The effect of GDC-0810 depends on the cellular context.

2019-07-25 | GSE128911 | GEO

ATAC-seq of MCF-7 cells post ligand treatment

Project description:Goal: study the impact of estrogen receptor ligands on chromatin accessibility in MCF-7 cells Methods: Assay for Transposase-Accessible Chromatin using Sequencing (ATAC-Seq) Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), significantly alters chromatin accessibility and partially mimics the effect of natural ligand E2 on chromatin accessibility in MCF-7 breast cells. Selective ER degraders (SERD) fulvestrant and GDC-0927 on the other hand have very little impact on chromatin accessibility.

2019-07-25 | GSE117940 | GEO

ChIP-seq of ER in MCF-7 cells post ligand treatment

Project description:Goal: study the impact of estrogen receptor (ER) ligands on ER binding to chromatin in MCF-7 cells Methods: ER Chromatin Immunoprecipitation and Sequencing (ChIP-seq) Results: All tested ligands increase binding of ER onto DNA in MCF-7 breast cells. These ligands thus promote an association between ER and DNA, irrespective of their mode of action: selective ER modulator (SERM) 4-OH tamoxifen, and selective ER degraders (SERD) fulvestrant and GDC-0927.

2019-07-25 | GSE117941 | GEO

RNA-seq of HCC1428 LTED breast cancer cell line post ligand treatment

Project description:Global gene expression analysis of HCC1428-LTED (long term estrogen deprived) breast cancer cell lines was evaluated after overnight treatment with 6 selective estrogen receptor degarders (SERDs). Two gene expression signatures were identified. GDC-0810 and AZD9496 have a similar gene expression profile which is distinct from fulvestrant. SAR439859 gene expression signature clusters closely with fulvestrant. Replacing the carboxylic side chain of GDC-0810 and AZD9496 with a basic side chain of SAR439859 to make novel SERDs, GDC-SAR and AZD-SAR, respectively, shifts the gene expression signature to more closely align to that of fulvestrant. The effect of SERDs on gene expression can be used to further differentiate classes of SERDs.

2020-07-10 | GSE154058 | GEO

ESR1 mutations maintain higher ER pathway activity relative to vehicle and ERa-WT controls following treatment with Raloxifene or fulvestrant.

Project description:The goal of the study was to understand whether mutations in ERa can promote resistance to various ERa antagonists of the SERD and SERM class. We found that ESR1 mutations can maintain higher ER pathway activity relative to control lines following short-term treatment with ERa antagonists raloxifene or fulvestrant.

2018-06-12 | GSE115564 | GEO

RNA-seq of 7 breast PDX models treated with Fulvestrant and AZD9833/camizestrant and collected at multiple timepoints

Project description:Oral selective estrogen receptor degraders (SERDs) could become the backbone endocrine therapy (ET) for estrogen receptor-positive (ER+) breast cancer, as they achieve greater inhibition of ER-driven cancers than current ETs and overcome key resistance mechanisms. This dataset was aimed at exploring the preclinical effects of the next-generation oral SERD camizestrant (AZD9833) on 7 PDX models. Mice were treated with fulvestrant or camizestrant for 4, 24, 48, 72 hours, with at least four replicates per condition.

2023-09-11 | E-MTAB-13139 | biostudies-arrayexpress

Neurofibromin is an Estrogen Receptor alpha Transcriptional Co-repressor in Breast cancer

Project description:We report that neurofibromin, a tumor suppressor and Ras-GAP (GTPase Activating Protein), is also an estrogen receptor-alpha (ER) transcriptional co-repressor through leucine/isoleucine-rich motifs that are functionally independent of GAP activity. GAP activity, in turn, does not impact ER binding. Consequently, neurofibromin-depletion causes estradiol hypersensitivity and tamoxifen agonism, explaining the poor prognosis associated with neurofibromin-loss in endocrine therapy-treated ER+ breast cancer. Neurofibromin-deficient ER+ breast cancer cells initially retain sensitivity to selective estrogen receptor degraders (SERDs). However, Ras activation does play a role in acquired SERD resistance, which can be reversed upon MEK inhibitor addition, and SERD/MEK inhibitor combinations induce tumor regression. Thus, neurofibromin is a dual repressor for both Ras and ER signaling, and co-targeting may treat neurofibromin-deficient ER+ breast tumors.

2020-02-14 | GSE142479 | GEO

RNA-sequencing of tamoxifen-resistant and -sensitive breast cancer cell lines.

Project description:We performed RNA-sequencing on 7 tamoxifen-resistant (MCF-7 Tam1, T-47D Tam1, T-47D Tam2, ZR-75-1 Tam1, ZR-75-1 Tam2, BT474 Tam1 and BT-474 Tam2) and their isogenic parental (MCF-7, T-47D, ZR-75-1 and BT-474) breast cancer cell lines. The tamoxifen-resistant cell lines were generated from the parentel cell lines by continuous administration of 1 µM 4-OH-tamoxifen for eight to twelve months. RNA- sequencing was performed to determine the changes in the expression of genes in the resistant clones as well as pathways. In addition, we compared the expression changes of the cell lines with those of the GSE58708 data set which we reanalyzied in our pipeline.

2018-08-30 | GSE111151 | GEO

Transcriptional profiling of Ishikawa cells treated with H3B-5942, E2, or standard of care compounds

Project description:The objective of this experiment was to determine the affect of H3B-5942 treatment on global gene expression in an estrogen-deprived setting (agonist mode) and to compare to treatment with a saturated analog of H3B-5942, GDC-0810, and standard of care agents tamoxifen and fulvestrant.

2018-06-12 | GSE115608 | GEO

RNA-seq of human breast cancer cell lines MCF7 and CAMA1 treated with Fulvestrant, AZD9496 and AZD9833/camizestrant, with and without estradiol

Project description:Oral selective estrogen receptor degraders (SERDs) could become the backbone endocrine therapy (ET) for estrogen receptor-positive (ER+) breast cancer, as they achieve greater inhibition of ER-driven cancers than current ETs and overcome key resistance mechanisms. This dataset was aimed at exploring the preclinical effects of the next-generation oral SERD camizestrant (AZD9833) on MCF7 and CAMA1 cell lines. Cells were treated with 1 nM estradiol and 100 nM fulvestrant, AZD9496, or camizestrant for 24 hours, with three replicates per condition and non-estradiol-treated controls.

2023-09-11 | E-MTAB-13113 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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