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T47D Breast cancer cell line ChIP-seq data

ABSTRACT: T47D Breast cancer cell line ChIP-seq data

PROVIDER: PRJNA415426 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6203180.fastq.gz	Fastqsanger.gz
	SRR6203181.fastq.gz	Fastqsanger.gz
	SRR6203178.fastq.gz	Fastqsanger.gz
	SRR6203179.fastq.gz	Fastqsanger.gz

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T47D Breast cancer cell line ChIP-seq data II

Project description:T47D Breast cancer cell line ChIP-seq data II

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T47D Breast cancer cell line ChIP-seq data

Project description:We performed genome-wide PADI2 ChIP seq experiments in T47D cell lines and also RNP2 ChIP seq in T47D cells only expressing HA Tagged amanitin resistant wild type in comparison to R1810A mutant form of RNAP2.

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aCGH hybridization of breast cancer cell line T47D

Project description:An array CGH hybridization of breast cancer cell line T47D compared against a normal human female reference.

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Project description:We report the comprehensive genome-wide binding peaks for key factors inovled in oxygen sensing pathways, such as HIF1α, HIF1β and EglN2. In addition, we also report the genome-wide binding peaks for NRF1 in breast cancer cells We conducted HA-EglN2, HIF1α, HIF1β (ARNT) or NRF1 ChIP-Seq in the T47D cell line that overexpresses HA-EglN2 in the presence of hypoxia (1%) and DMOG treatment. T47D parental cells treated with the same condition followed by HA ChIP-seq served as the control to filter non-specific binding.

2014-07-31 | E-GEOD-59935 | biostudies-arrayexpress

T47D Breast cancer cell line ChIP-seq data II

Project description:We performed genome-wide CDK9 ChIP seq experiments in T47D cells only expressing HA Tagged amanitin resistant wild type in comparison to R1810A mutant form of RNAP2.

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Project description:Inhibitors for cyclin-dependent kinase (CDK) 4 and CDK6 have been established as effective therapeutic options for hormone receptor (HR)-positive, HER2-negative advanced breast cancer. Although the CDK4/6 inhibitors mainly target the cyclin D-CDK4/6-retinoblastoma tumor suppressor protein (RB) axis, little is known about clinical impact of inhibiting phosphorylation of other CDK4/6 target proteins. Here, we have focused on other CDK4/6 targets, SMAD proteins. We showed that a CDK4/6 inhibitor Palbociclib and Activin-SMAD2 signaling cooperatively inhibited cell cycle progression of a luminal-type breast cancer cell line T47D. Mechanistically, Palbociclib enhanced SMAD2 binding to the genome through inhibiting linker phosphorylation of the SMAD2 protein by CDK4/6. Comparison of the SMAD2 ChIP-seq data of T47D with those of a triple-negative breast cancer cell line Hs578T indicated that Palbociclib augments different SMAD2-mediated program defined based on types of cells, and enhances SMAD2 binding to the target regions on the genome without affecting its binding pattern. Collectively, the CDK4/6 inhibitor facilitates the cytostatic effects of Activin-SMAD2, while it also enhances its tumor promoting effects depending on types of breast cancer.

2018-10-23 | GSE117495 | GEO

Baseline Expression of Inflammatory Cytokines and Receptors in the T47D Human Breast Cancer Cell Line

Project description:Immortalized human breast cancer cell line, T47D, was analyzed via RT-qPCR for transcript expression of selected inflammatory cytokines and cytokine receptors associated with promotion of tumor vasculature and breast cancer metastasis

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Phosphoproteomics of BYL719 (alpelisib)-Resistant T47D Human Breast Cancer Cell Line

Project description:The PI3Kalpha-specific inhibitor Alpelisib (BYL719) has been approved for the treatment of metastatic ER+/HER2- breast cancer patients in combination with Fulvestrant. After initial response, patients develop drug resistance and disease relapses. In order to identify signalling pathways contributing to the acquired resistance to BYL719 in breast cancer, we generated BYL719-resistant T47D cells and used them together with the parental cells to perform label-free quantitative phosphoproteomics.

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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.

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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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