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Transcriptome profile of breast cancer HS-578T cells overexpressing EP300

ABSTRACT: HS-578T cells overexpressing EP300 show an increase in doxorubicin and paclitaxel resistance, up-regulation of EMT markers together with an increase in motility and invasion, and an increase in the percentage of cancer stem cells and mammosphere formation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE116370 | GEO | 2019/03/19

REPOSITORIES: GEO

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Transcriptome profile of breast cancer HS-578T cells overexpressing EP300

Project description:Transcriptome profile of breast cancer HS-578T cells overexpressing EP300

| PRJNA478310 | ENA

Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [RNA-Seq2]

Project description:Purpose:Assess the difference in gene expression of taxol-resistant TNBC cells relative to parental cells (MDA-MB-436 and HS 578t) Methods: RNA-seq was performed on paclitaxel-treated MDA-MB-436 cells that are resistant to Paclitaxel (R20A, R20B, R20C) and in control-treated (DMSO) parental MDA-MB-436 cells that are sensitive to Paclitaxel (DMSO) Results: We mapped about 20 million sequence reads per sample to the human genome (hg19) and identified identified differentially expressed genes Conclusions: Our study identified genes significantly enriched or repressed in taxol-resistant cells relative to parental cells in both TNBC models (MDA_MB-436 and HS 578T)

2020-08-18 | GSE113685 | GEO

Gene Expression Pattern in EP300 knocked-down MCF7 cells and corresponding paclitaxel resistant derivatives

Project description:EP300, a transcriptional co-activator of E-cadherin, has been recently found by our group to regulate doxorubicin resistance via by-pass of senescence and paclitaxel resistance by overcoming apoptosis in a minimally transformed mammary epithelial cells (MTMEC). Moreover, EP300 deleted MTMEC cells exhibit an multi-drug resistant (MDR) phenotype independent of P-glycoprotein (ABCB1), an efflux pump or ABC drug transporter. This whole transcriptome array study was undertaken in order to explore the downstream targets in the EP300-mediated drug resistance, epidermal-to-mesenchymal transition and cancer stem cell phenotypes in breast cancer cell line MCF7.

2017-06-13 | GSE76200 | GEO

Transcription profiling of human Hs 294T cells treated with elesclomol alone or in combination with paclitaxel compared to DMSO treated

Project description:We used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with paclitaxel, to aide in identifing the mechnism of action of elesclomol. Experiment Overall Design: Hs 294T human melanoma cells were grown in vitro. They were seeded at a low density and were left untreated, treated with the vehicle, treated with elesclomol, treated with paclitaxel, or treated in combination with both elesclomol and paclitaxel. They were incubated for 6 hours before harvesting.

2008-06-19 | E-GEOD-11550 | biostudies-arrayexpress

Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [RNA-Seq1]

Project description:Purpose:Assess the difference in gene expression of taxol-resistant TNBC cells relative to parental cells (MDA-MB-436 and HS 578T) upon treatment with UNC1999 3uM Conclusions: Our study identified genes significantly enriched or repressed in taxol-resistant cells relative to parental cells in both TNBC models (MDA_MB-436 and HS 578T)

2020-08-18 | GSE111920 | GEO

Comparison between Saccharomyces cerevisiae HS 10, HS 34 and HS 12, HS 37

Project description:Gene expression of different flocculent (HS 10 and HS 34) and powdery (HS 12 and HS 37) yeast strains compared to each other during exponential and stationary growth phase was analysed. The isolation of RNA was done by disruption of the cells under liquid nitrogen using mortar and pistil and then the Qiagen RNeasy Midi Kit with some modifications within the manufacturers´ protocol and the Qiagen RNase-Free DNase Set were applied. 6 µg of the total RNA per sample was used for each microarray experiments. The indirect labelling by the tyramide-signal-amplification method (MicromaxTM TSATM labelling and detection Kit from Perkin Elmer life sciences) was used to increase the Cy3 and Cy5 signals of microarray detection. Each cDNA containing Biotin- and Fluorescein-nucleotides respectively was purified with a QIAquick PCR purification kit and suspended in 11 µl of the formamide containing hybridization buffer. The slides were hybridized at 42°C over night under a cover slip. The microarrays were scanned by the Axon 4000B scanner; image intensity data were extracted and analysed with GenePix® Pro 6.0 software. Data from different scans of Dye-swap experiment were extracted by GenePix Pro 6.0 software, normalized and united. An outliertest has been applied in order to find outliers amongst the gene replicats. Subsequently, a t-test (1% and 5% probability of error) has been used in order to find regulated genes. Keywords: sorted yeast cells Microarray experiments were realised with dye swap.

2008-12-11 | E-GEOD-12369 | biostudies-arrayexpress

Hs 294T Cells Treated with Elesclomol Alone or in Combination with Paclitaxel Compared to DMSO Treated

2008-05-29 | GSE11550 | GEO

Comparison between Saccharomyces cerevisiae HS 10, HS 34 and HS 12, HS 37

2008-12-12 | GSE12369 | GEO

SAGE-Seq gene expression profiles of Hs578T, MCF7, and SUM159PT cells treated with STAT3 or non-targeting siRNAs, DMSO, or CXCR2, PTGIS, HAS1, PFKFB3, JAK, or NQO1 inhibitor

Project description:To investigate potential links between Stat3 transcriptional activity and other signaling pathways in breast cancer, we determined the gene expression profiles of three breast cancer cell lines treated with JAK, PTGIS, PFKFB3, CXCR2, HAS1, or NQO1 inhibitor (all of which decreased Stat3 transcriptional activity in Hs 578T cells except for the NQO1 inhibitor), inhibitor treatment vehicle alone (DMSO), STAT3 siRNAs, or non-targeting siRNAs. Using the resulting data, we identified a gene signature that was significantly regulated by STAT3 siRNAs and similarly affected by the JAK and at least 3 other inhibitors (or by 4 other inhibitors) but not by the NQO1 inhibitor in Hs 578T cells that was enriched in genes involved in development and correlated with shorter distant metastasis-free survival in primary lymph-node-negative invasive breast tumors. These results emphasize the central importance of Stat3 in CD44+/CD24- stem-cell-like breast cancer cells. This study includes SAGE-Seq libraries obtained using 27 samples that each underwent individual protocols. There are nine samples of each of three cell lines - Hs 578T, MCF7, and SUM159PT. The samples in each group were treated with either one of the six inhibitors, DMSO only (the background control for inhibitor-treated cells), STAT3 siRNAs, or non-targeting siRNAs (the background control for STAT3 siRNAs).

2011-09-08 | E-GEOD-22917 | biostudies-arrayexpress

Expression data from WT, Crebbp+/- and Ep300+/- bone marrow stroma

Project description:We found that the bone marrow microenvironment of Crebbp+/- mice was unable to properly maintain the immature stem - and progenitor pools. Instead, it stimulates myeloid differentiation that progresses into a myeloproliferative-like disease. Since CREBBP is a transcriptional co-activator, we used gene expression analysis to globally assess functional deficiencies in Crebbp+/- bone marrow stroma cells at a molecular level. Ep300 encodes a protein which is highly similar in structure and function to CREBBP; nevertheless, Ep300+/- mice suffer neither excessive myeloid differentiation nor loss of HSCs. Therefore, to identify expression changes specifically related to Crebbp heterozygosity, we focused on genes that showed significant differences in expression levels between Crebbp+/- and wild-type bone marrow stroma but no difference between Ep300+/- and wild-type. Bone marrow stroma was established from wild-type, Crebbp+/- and Ep300+/- mice that were 3-4 months old for RNA extraction and hybridization on Affymetrix microarrays. There are 4 biological replicates for each genotype used.

2011-03-01 | E-GEOD-24773 | biostudies-arrayexpress

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