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Effect of diptoindonesin G on T47D cells overexpressing the Y537S ER mutation

ABSTRACT: Effect of diptoindonesin G on T47D cells overexpressing the Y537S ER mutation

PROVIDER: PRJNA847231 | ENA |

REPOSITORIES: ENA

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Effect of diptoindonesin G on T47D cells overexpressing the Y537S ER mutation

Project description:To investigate the effect of diptoindonesin G on breast cancer cells expressing the estrogen receptor Y537S ligand binding domain mutation, we treated T47D cells overexpressing the ER Y537S mutation and treated them with vehicle or diptoindonesin G and performed differential gene expression analysis and gene set enrichment analysis

2022-06-11 | GSE205716 | GEO

RNA-seq data of T47D overexpressing prolactin and the control

Project description:The exact role of prolactin on breast cancer still remains unclear. Clues supportive or unsurpportive for prolactin to be cancer driver are confusing. To clarify the role of autocrine prolactin of breast cancer cells on cancer development, we construct T47D cells overexpressing prolactin.

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Transriptome profiling of breast cancer cells T47D overexpressing ZNF528-AS1

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ER/PR RIME Experiments in MCF7 and T47D cell lines

Project description:Immuno-precipitation followed by MS was performed using the RIME protocol in this study. Estrogen Receptor (ER) and Progestorone Receptor (PR) were targetted using antibodies. The experiments were performed in a quantitative manner using SILAC labelling. Cells grown in complete serum (estrogenic) conditions were compared against an cells in similar complete media, however supplemented with Progesterone (PG) or R5020 for 4 hours. Experiments were performed in MCF7 and T47D cell lines

2015-05-26 | PXD002104 | Pride

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

Transriptome profiling of breast cancer cells T47D overexpressing ZNF528-AS1

Project description:Transriptome profiling of breast cancer cells T47D overexpressing ZNF528-AS1

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miRNA Expression data from WASF3 overexpressing stable T47D cells and control cells

Project description:We recently showed that inactivation of the WASF3/WAVE3 gene in breast cancer cells results in loss of cell motility and invasion in vitro and metastasis in vivo. To obtain a better understanding of molecular mechanisms of action of WASF3, we have established the stable WASF3 overexpressing T47D cells using lentiviral infect system. We used miRNA microarrays to detail the global programme of miRNA expression after overexpression of WASF3 and identified distinct classes of up or down-regulated metastmir associated with breast cancer cell migration and motility invasion

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T47D shNT versus T47D shRON

Project description:T47D shNT versus T47D shRON

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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 .

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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 ERα-positive tumors exhibit intrinsic or rapidly acquire resistance to endocrine treatment, requiring chemotherapy. Ιt 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.

2014-08-29 | GSE60878 | GEO

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