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RNA-seq analysis of hormone receptor positive breast cancer cell line T47D with 24h hormone treatment

ABSTRACT: RNA-seq analysis of hormone receptor positive breast cancer cell line T47D with 24h hormone treatment

PROVIDER: PRJNA807652 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18052119_1.fastq.gz	Fastqsanger.gz
	SRR18052119_2.fastq.gz	Fastqsanger.gz
	SRR18052120_1.fastq.gz	Fastqsanger.gz
	SRR18052120_2.fastq.gz	Fastqsanger.gz
	SRR18052121_1.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of hormone receptor positive breast cancer cell line T47D with 24h hormone treatment

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RNA-seq analysis of hormone receptor positive breast cancer cell line UCD4 with 24h hormone treatment

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SMAD2 binding regions in estrogen receptor-positive breast cancer cell line, T47D

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.

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RNA-seq analysis of hormone receptor positive breast cancer cell line UCD4 with 24h hormone treatment

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Efficacy of abemaciclib in palbociclib-resistant hormone receptor positive breast cancer cell lines: MCF-7 and T47D

Project description:Efficacy of abemaciclib in palbociclib-resistant hormone receptor positive breast cancer cell lines: MCF-7 and T47D

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SMAD2 binding regions in estrogen receptor-positive breast cancer cell line, T47D

Project description:SMAD2 binding regions in estrogen receptor-positive breast cancer cell line, T47D

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Preoperative short-term hormone therapy for hormone receptor positive breast cancer

Project description:Core needle biopsy (Cx) primary cancer specimens were collected at Okayama University Hospital in Japan from hormone receptor positive /HER2 negative patients that subsequently received two weeks of neoadjuvant hormone therapy. Thirty clinical TNM stage I and II women were enrolled in this study. The study was approved by the Institutional Review Board and all patients signed informed consent forms. Patients received preoperative hormone therapy daily for two weeks before surgery. Premenopausal patients received tamoxifen (40 mg) and postmenopausal patients received letrozole (2.5 mg). All patients underwent a mastectomy or breast-conserving surgery. Surgical samples after treatment were also collected. Hormone and HER2 receptor statuses were determined in the diagnostic Cx specimens before hormone therapy. Cases with ≥1% positive nuclear staining for estrogen receptors (ER) or progesterone receptors (PgR) with IHC were considered hormone receptor-positive. Cases with either 0 or 1 positive IHC staining for HER2 or with an HER2 gene copy number < 2.0 by fluorescent in situ hybridization (FISH) analysis were considered HER2−. Specimens for gene expression analysis were collected into RNA and later stored at -80°C. Gene expression profiling was performed using Affymetrix U133A gene chips. Expression data were normalized using the MAS5 algorithm, mean centered to 600, and log2 transformed before further analysis.

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T47D cell line transfected with various ESR1 fusion genes (or with estrogen treatment), vs. YFP transfection alone

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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).

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