Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

90 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from Tamoxifen resistant Breast Cancer Cell lines

ABSTRACT: Tamoxifen Resistant (TR) gene profile from Breast cancer cell lines T47D and ZR75-1 with their oestrogen-deprieved conterparts were analysed for gene associated with TR. We used Microarray Affymetrix HU133plus 2.0 chips for gene expression of TR cell lines, normalised them against GEO data available for normal T47D (GSM70667) and ZR75-1 (GSM70668). We grew parental breast cancer cell lines in tamoxifen containing media (0.1 microM) for 6 months and labelled them tamoxifen resistant (TR). Oestrogen-Deprieved cells were grown in charcoal-stripped media for 6 months then tamoxifen (0.1 microM) was added to the media and cells maintained a further 6 months and termed Oestrogen deprieved-tamoxifen resistant (ODTR) .

ORGANISM(S): Homo sapiens

SUBMITTER: Helen Hurst

PROVIDER: E-GEOD-22664 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

Expression data from Tamoxifen resistant Breast Cancer Cell lines

Project description:Tamoxifen Resistant (TR) gene profile from Breast cancer cell lines T47D and ZR75-1 with their oestrogen-deprieved conterparts were analysed for gene associated with TR. We used Microarray Affymetrix HU133plus 2.0 chips for gene expression of TR cell lines, normalised them against GEO data available for normal T47D (GSM70667) and ZR75-1 (GSM70668).

2010-12-31 | GSE22664 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of human breast cancer cell T47D and T47D-TR Transcriptomes

Project description:To gain new insight into the resistance to hormonal therapy in breast cancer, we generated a tamoxifen-resistant human breast cancer cell line T47D-TR by exposing estrogen-sensitive cell line T47D to increasing concentrations of 4-hydroxy tamoxifen (4-OHT) and identified its resistance with different ways. What we interested is the underlying mechanisms of breast cancer tamoxifen resistance which was not reported yet.Here, we detect the RNA sequence of both the two cell lines hoping to find some evidence.

2020-01-28 | GSE125738 | GEO

RIME against TRPS1 in breast cancer cell lines

Project description:Identification of TRPS1 interactors in MCF7, T47D and ZR75-1 breast cancer cell lines.

2018-06-12 | PXD009863 | Pride

Expression data from T47D/S2 (control) and T47D/TR-2 (tamoxifen-resistant) cell lines

Project description:Expression data from T47D/S2 (control) and T47D/TR-2 (tamoxifen-resistant) cell lines

| PRJNA914306 | ENA

Effect of tamoxifen on early gene expression in T47D cells

Project description:Tamoxifen is the treatment of choice in estrogen receptor alpha breast cancer patients. However, ~50% of ERM-NM-1-positive tumors exhibit intrinsic or rapidly acquire resistance to endocrine treatment, requiring chemotherapy. M-NM-^Yt has been difficult to predict de novo resistance to endocrine therapy and/or assess the likelihood of early relapse, while no concrete mechanism regulating the acquisition and the maintenance of endocrine resistance has been identified. We have performed a whole transcriptome analysis of an ER-positive (T47D) and a triple-negative (MDA-MBA-231) breast cancer cell line exposed to tamoxifen for a short time frame (hours) in order to study resistance mechanisms that are initiated early after initiation of tamoxifen treatment. Cells after a 4h incubation with medium containing 10% charcoal stripped FBS were incubated with vehicle, E2 (10-6M) or tamoxifen (10-6M) in RPMI 1640 supplemented with 10% charcoal stripped FBS, for 3 hours. Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturerM-bM-^@M-^Ys instructions. RNA was labeled and hybridized according to the Affymetrix protocol (Affymetrix Gene-Chip Expression Analysis Technical Manual), using the HGU133A plus 2 chip, analyzing a total of 54675 transcripts. Signals were detected by an Affymetrix microarray chip reader.

2014-08-29 | E-GEOD-60878 | biostudies-arrayexpress

The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer. [human]

Project description:The ets transcription factor ELF5 specifies the differentiation of mammary progenitor cells to establish the milk-secreting lineage. ER- and poor prognosis basal breast cancers arise from this progenitor cell and these cancers express high levels of Elf5. Knockdown of ELF5 expression in basal breast cancer cell lines, or forced expression in luminal breast cancer cell lines, resulted in reduced cell proliferation. Transcript profiling and chromatin immunoprecipitation revealed that the transcriptional activity of ELF5 specified the gene expression patterns that distinguish basal from luminal breast cancer, including suppression of FOXA1, GATA3 and ER, key estrogen-action genes. Tamoxifen treatment of luminal MCF7 cells upregulated Elf5 expression and cells that acquired resistance to Tamoxifen became dependent on ELF5 for proliferation. ELF5 is a regulator of breast cancer cell proliferation, transcriptionally specifies the basal molecular subtype and is utilised by ER+ breast cancer cells to escape proliferative arrest caused by Tamoxifen. Elf5 was knocked down via siRNA in basal HCC1937 cell lines, in triplicate. Elf5 was induced in luminal T47D and MCF7 cell lines via a doxycycline inducible expression vector, in duplicate.

2012-12-27 | E-GEOD-30405 | biostudies-arrayexpress

Effect of estradiol and tamoxifen on SPEN-expressing and control T47D cells.

Project description:Split Ends (SPEN) is a transcriptional coregulator that have formerly identified as a tumour suppressor gene in ER-positive breast cancers. However, ER-positive breast cancers are diagnosed at similar frequencies in pre- and post-menopausal women who show significantly different circulating hormone levels. This therefore raises the possibility that SPEN functions under hormone-depleted settings may contrast with its roles in the presence of hormones. We therefore attempted to explore the cellular functions regulated by SPEN under hormone-depleted settings using a previously established model with T47D cells stably transfected with a control vector (non-target) or SPEN-expressing vector. In particular, we attempted to investigate the hormone-independent transcriptional program regulated by SPEN in breast cancer. To achieve this, we have treated previously established T47D cells stably transfected with a control vector (non-target) or SPEN-expressing vector. These cells were allowed to grow in hormone-depleted conditions for 4 days. To minimize external biases introduced by hormone depletion or any transcriptional contribution from the estrogen receptor (ER), we also performed gene expression profiling analyses on the same cells but stimulated with an estrogen receptor (ER) agonist (Estradiol) or antagonist (Tamoxifen).

2017-08-15 | E-MTAB-4975 | biostudies-arrayexpress

RNA-seq of human breast cancer cell line T47D and 2 different T47D_H2A.J-KO cells lines treated with tamoxifen and untreated controls

Project description:The experiment is intended to test the effect of the Cripsr/Cas9 deletion of the H2AFJ gene encoding the histone variant H2A.J on the transcriptome of luminal breast cancer T47D cells in conditions of proliferation, and after proliferative arrest induced by treating the cells with 5 µm tamoxifen for 4 days. Two independent H2A.J-KO cell lines were analyzed: KO1 and KO18.

2021-09-20 | E-MTAB-10861 | biostudies-arrayexpress

Actions of tamoxifen in the uterus and its molecular effectors in endometrial carcinogenesis.

Project description:The molecular explanation for tamoxifen serving as a breast cancer treatment but displaying partial estrogenic in the uterus is not known. Previously, we reported that differential promoter context and cofactor recruitment contribute to the tissue specificity of tamoxifen. Here, we investigated the genomic basis for the partial oestrogenic activity of tamoxifen in the endometrium. We showed that tamoxifen not only affects the rate of transcription of oestrogen target genes but also targets a unique set of genes. Since oestrogen and tamoxifen are both able to bind to oestrogen receptors (ERs) and because both promote endometrial carcinogenesis, we hypothesized that the molecular effectors for ERs in endometrial carcinogenesis most likely reside in genes that are commonly targeted by oestrogen and tamoxifen. Among those target genes, we identified a paired-box gene PAX2 that is critically involved in cell proliferation and carcinogenesis in the endometrium. Our experiments also demonstrated that PAX2 is activated by oestrogen and tamoxifen in endometrial carcinomas but not in normal endometrium, and this activation is associated with cancer-linked hypomethylation of the PAX2 promoter. Keywords: actions of tamoxifen

2005-07-29 | GSE3013 | GEO

RNA-seq of human breast cancer cell lines MCF7 and T74D naive and resistant to palbociclib treated with capivasertib, fulvestrant and combination

Project description:T47D and MCF7 cell lines were treated with long-term (continuous) palbociclib to induce 4 resistant cell-lines (T47D RB-, T47D CDK6H, MCF7 RB- and MCF7 PacqR). Each cell line (both parental and resistant) were then treated with DMSO (control), capivasertib monotherapy, fulvestrant monotherapy and capivasertib/fulvestrant combination. RNA data is available after each treatment and resistant cell lines additionally have RNA data available after continuous palbociclib treatment.

2023-08-14 | E-MTAB-13262 | 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