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SMAD2 binding regions in breast cancer cell line and RNA-seq transcriptome analyses in T47D

ABSTRACT: SMAD2 binding regions in breast cancer cell line and RNA-seq transcriptome analyses in T47D

PROVIDER: PRJNA482337 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7550970.fastq.gz	Fastqsanger.gz
	SRR7550980.fastq.gz	Fastqsanger.gz
	SRR7550971.fastq.gz	Fastqsanger.gz
	SRR7550981.fastq.gz	Fastqsanger.gz
	SRR7550972.fastq.gz	Fastqsanger.gz

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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.

2018-10-23 | GSE117495 | GEO

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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SMAD2 binding regions in triple negative breast cancer cell line, Hs578T

2018-10-23 | GSE117496 | GEO

RNA-seq transcriptome analyses in T47D cells treated with ActA and Palbociclib.

Project description:We performed SMAD2 ChIP-seq analysis in T47D cells with/without Palbociclib treatment. To validate whether the changes in SMAD2 binding to the genome indeed resulted in changes in target gene expression, we performed RNA-seq transcriptome analyses in T47D with/without ActA stimulation and Palbo treatment.

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Smad2/3 binding regions in NMuMG cells

Project description:Smad2/3 binding regions in NMuMG cells

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Smad2/3 binding regions in NMuMG cells

Project description:Smad2/3 binding regions in mouse mammary gland epithelial cells (NMuMG) treated with TGF-beta for 1.5 h were determined by ChIP-seq to evaluate the transcriptional mechanism of TGF-beta-Smad signaling.

2019-08-29 | GSE121254 | GEO

SMAD2 binding regions in triple negative breast cancer cell line, Hs578T

Project description:SMAD2 binding regions in triple negative breast cancer cell line, Hs578T

| PRJNA482343 | ENA

SMAD2 binding regions in breast cancer cell line and RNA-seq transcriptome analyses in T47D

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-10-23 | GSE117502 | GEO

Smad2/3 binding sites in HaCaT, HepG2, and Hep3B cells determined by an Affymetrix promoter array

Project description:Specific regulation of target genes by transforming growth factor-β (TGF-β) in a given cellular context is determined in part by transcription factors and cofactors that interact with the Smad complex. In the present study, we determined Smad2 and Smad3 (Smad2/3) binding regions in the promoters of known genes in HepG2 hepatoblastoma cells, and compared them to those in HaCaT epidermal keratinocytes to elucidate the mechanisms of cell-type- and context-dependent regulation of transcription induced by TGF-β. Our results show that 81% of the Smad2/3 binding regions in HepG2 cells were not shared with those found in HaCaT cells. Hepatocyte nuclear factor 4α (HNF4α) is expressed in HepG2 cells, but not in HaCaT cells, and the HNF4α binding motif was identified as an enriched motif in the HepG2-specific Smad2/3 binding regions. ChIP-sequencing analysis of HNF4α binding regions under TGFα stimulation revealed that 32.5% of the Smad2/3 binding regions overlapped HNF4α bindings. MIXL1 was identified as a new combinatorial target of HNF4α and Smad2/3, and both the HNF4α protein and its binding motif were required for the induction of MIXL1 by TGF-β in HepG2 cells. These findings generalize the importance of binding of HNF4α on Smad2/3 binding genomic regions for HepG2-specific regulation of transcription by TGF-β, and suggest that certain transcription factors expressed in a cell-type-specific manner play important roles in the transcription regulated by the TGF-β-Smad signaling pathway.

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Genome-wide maps of SMAD2-chromatin binding state in TGFbeta-treated vascular smooth muscle cells

Project description:To further explore the role of these two factors in SMC reprogramming, we treated human aortic smooth muscle (HASMCs) in vitro with TGFβ and mapped binding of Smad2/3, which reflects TGFβ activity, and Pol2-Ser2p, which reflects transcriptional activity, by ChIP-seq analysis. Smad2/3 bound to numerous regulatory regions in the genome differentially regulating expression of numerous genes as demonstrate by alterations in Pol2-Serp2 binding profile and analysis of bulk RNA sequencing. Examination of the top 20 transcription factors identified by sequencing of Smad2/3 binding regulatory regions identified KLF4 gene as one of the most prominently regulated genes. Further analysis showed Smad2/3 binding to multiple KLF4 gene regulatory elements that increased following TGFβ treatment, indicating that KLF4 is a direct target of Smad2/3. At the same time, the amount of bound Pol2-Ser2p decreased, pointing to reduced transcriptional activity. In contrast, Smad2/3 did not bind to KLF2 or KLF5 regulatory elements, demonstrating that these genes are not directly regulated by TGFβ.

2018-03-27 | GSE112326 | GEO

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