Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA326980 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3723530.fastq.gz | Fastqsanger.gz | |||
| SRR3723531.fastq.gz | Fastqsanger.gz | |||
| SRR3723532.fastq.gz | Fastqsanger.gz |
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Project description:We performed SMAD2/3 ChIP-seq analysis in MCF10A MII cells. To validate whether the changes in SMAD2/3 binding to the genome indeed resulted in changes in target gene expression, we performed RNA-seq transcriptome analysis after short and long periods of TGFβ stimulation (0, 1.5h and 16h) in MII cells. In addition, we revealed that JUNB is a critical AP1 component for SMAD2/3 binding after TGFβ stimulation. To assess the significance of JUNB for TGFβ-SMAD-target genes on a genome-wide scale, we also performed RNA-seq transcriptome analysis in JUNB-knock-downed MII cells.
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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.
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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.
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Project description:SMAD2/3 binding pattern in triple-negative breast cancer cell lines, Hs578T and BT549 [ChIP-seq]
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Project description:In this study, we took advantage of a previously established breast cancer progression cell line model system, which consists of a parental MCF10A (MI) spontaneously immortalized mammary epithelial cell line and two of its derivatives: 1) MCF10ATk.cl2 (MII), a MCF10A H-Ras transformed cell line and 3) MCF10CA1h (MIII), derived from a xenograft of the MII cells in nude mice that progressed to carcinoma (1, 2). These cell lines were previously reported to exhibit distinct tumorigenic properties when re-implanted in nude mice; MI is non-tumorigenic, MII forms benign hyperplastic lesions and MIII forms low-grade, well differentiated carcinomas (2, 3). The advantage of this system is that these cell lines were derived from a common genetic background (MCF10A) and accumulated distinct genetic/epigenetic alterations in vivo enabling them to acquire a range of non-tumorigenic to carcinogenic properties. Our initial studies showed that MIII cells, but not MI or MII, exhibit an EMT phenotype, promoter DNA hypermethylation of epithelial genes and highly invasive properties in vitro. To investigate the role of TGFβ pathway in these processes, we disrupted the TGFβ downstream signaling events in MIII, by stably overexpressing the inhibitory Smad7, and analyzed the gene expression profiles of MII, MIII and MIIISmad7 cells using microarray analysis. Total RNA was isolated from three biological replicates corresponding to MIIpB, MIIIpB and MIIIpB-Smad7 cells using Trizol (Invitrogen) according to the manufacturer’s protocol, and the RNeasy mini-kit (Qiagen) was used to clean-up the RNA. Labeled cRNA fragments derived from the samples were hybridized onto human genome U133 plus 2.0 arrays (Affymetrix). Gene-expression estimates and a measure of sequence-specificity of the hybridization intensities were both determined using standard settings in MAS5 (Affymetrix). Probesets that did not exhibit sequence-specific hybridization in any sample were excluded from subsequent analysis. Differential expression between MIIpB and MIIIpB as well as between MIIIpB and MIIIpBSmad7 was assessed using Student’s t-test. Genes with a false discovery rate (FDR) < 0.05 and a greater than 2-fold difference in expression between the two cell lines were considered to be differentially expressed.
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