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Unknown,Transcriptomics,Genomics,Proteomics

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EpCAM expressing Hs578T cells

ABSTRACT: EpCAM is frequently overexpressed in human invasive breast cancer. We reported EpCAM overexpression to be an independent prognostic marker for poor overall survival in node-positive breast cancer. We used microarrays in order to investigate changes of the transcriptome on EpCAM gene overexpression in human breast cancer cells Hs578T cells were found to express only very little EpCAM mRNA and protein in comparison to established and well characterized breast cancer cell lines such as MCF-7 or SK-BR-3. Hs578T cells were stably transfected with the EpCAM cDNA containing construct pIRESpuro3_EpCAM and the respective empty vector control.

ORGANISM(S): Homo sapiens

SUBMITTER: Gilbert Spizzo

PROVIDER: E-GEOD-25743 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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EpCAM expressing Hs578T cells

Project description:EpCAM is frequently overexpressed in human invasive breast cancer. We reported EpCAM overexpression to be an independent prognostic marker for poor overall survival in node-positive breast cancer. We used microarrays in order to investigate changes of the transcriptome on EpCAM gene overexpression in human breast cancer cells

2010-12-02 | GSE25743 | GEO

RNA-seq in Hs578T cells stimulated with TGF-β

Project description:Transforming growth factor-β (TGF-β) comprises a key component in the tumor microenvironment. It is reported that TGF-β can be pro-tumorigenic or anti-tumorigenic depending on various contexts. Some of the triple negative breast cancers highly express TGF-β, but pro-tumorigenic function of TGF-β in triple negative breast cancer cells is not fully known. Therefore, we analyzed genome-wide gene expression changes after stimulation with TGF-β in a triple negative breast cancer cell line, Hs578T cells.

2020-12-24 | GSE152414 | GEO

ChIP-sequencing of ZEB1 in triple negative breast cancer cell line Hs578T

Project description:This experiment is performed to reveal the novel binding sites of ZEB1 transcription factor globally in triple negative breast cancer cell line Hs578T. We also reveal the effect of TGF cytokine on the binding sites of ZEB1.

2018-04-25 | E-MTAB-5241 | biostudies-arrayexpress

ChIP-sequencing of Snai1 transcription factor in triple negative breast cancer cell line Hs578T

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Role of CCN3 on Hs578T triple negative breast cancer cell line

Project description:Transcriptome sequencing analysis of Hs578T control (CTRL sh) and CCN3 knockdown (CCN3 sh) cell lines. CCN3, also known as nephroblastoma overexpressed (NOV, NOVH), has been associated with cell migration, invasion, angiogenesis, adhesion and proliferation in several cancer types like Ewing’s sarcoma, glioma, prostate cancer, hepatocellular carcinoma, clear cell renal cell carcinoma, chondrosarcoma and melanoma. These results provide information about gene expression affected by CCN3 in triple-negative breast cancer cell lines.

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FBP1 expression in basal-like breast cancer MDA-MB231 and Hs578T cells

Project description:FBP1 is a rate limiting enzyme in glucogenogenesis and FBP1 expression changes cells to oxidative phosphorylation. Expressing FBP1 in basal-like breast cancer cells, which lack the expression of this enzyme, will identify the genes involved in glycolysis. FBP1 was expressed in MDA-MB231 and Hs578T cells, stable clones were selected, and RNA was prepared for microarray analysis.

2012-09-27 | E-GEOD-41158 | biostudies-arrayexpress

Homo sapiens

Project description:EpCAM expressing Hs578T cells

| PRJNA134095 | ENA

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

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 | GSE117496 | GEO

DNA methylation analysis of breast cancer Hs578T cells with TET1 knockout

Project description:DNA methylation analysis of breast cancer Hs578T cells with TET1 knockout

| PRJNA475774 | ENA

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