Similar Datasets
Project description:The effects of SNAI2 overexpression on the transcriptional program in HaCaT cells
| PRJNA699576 | ENA
Project description:Investigation of the transcriptional profile of TGF-β1-induced EMT in HaCaT cells.
2021-09-01 | GSE166200 | GEO
Project description:1. Keratinocytes infected with retroviruses expressing control or SNAI2 shRNAs were cultured in growth medium and Affymetrix HG-U133 plus 2.0 arrays were used to determine global gene expression profiles. 2. Keratinocytes infected with retroviruses overexpressing LACZ or SNAI2 were cultured in growth medium and Affymetrix HG-U133 plus 2.0 arrays were used to determine global gene expression profiles. Keratinocytes with knockdown or overexpression of SNAI2 were used to determine gene expression profiles
2014-10-15 | E-GEOD-55269 | biostudies-arrayexpress
Project description:1. Keratinocytes infected with retroviruses expressing control or SNAI2 shRNAs were cultured in growth medium and Affymetrix HG-U133 plus 2.0 arrays were used to determine global gene expression profiles. 2. Keratinocytes infected with retroviruses overexpressing LACZ or SNAI2 were cultured in growth medium and Affymetrix HG-U133 plus 2.0 arrays were used to determine global gene expression profiles.
2014-10-15 | GSE55269 | GEO
Project description:We report the ChIP-Seq results of SNAI2 in several different conditions which include: SNAI2 binding in both control and SNAI2 knockdown cells to demonstrate specificity of the binding. SNAI2 ChIP-Seq was also performed in SNAI2 or control LACZ overexpressing cells cultured in growth medium as well as LACZ or SNAI2 overexpressing cells in differentiation medium.
2014-10-15 | GSE55421 | GEO
Project description:We report the ChIP-Seq results of SNAI2 in several different conditions which include: SNAI2 binding in both control and SNAI2 knockdown cells to demonstrate specificity of the binding. SNAI2 ChIP-Seq was also performed in SNAI2 or control LACZ overexpressing cells cultured in growth medium as well as LACZ or SNAI2 overexpressing cells in differentiation medium. Examination of SNAI2 binding sites across the genome using the 6 different conditions
2014-10-15 | E-GEOD-55421 | biostudies-arrayexpress
Project description:Aim of the study was to characterize at a molecular level (changes in transcriptomes) the effect of monosodium urate crystal (MSU) on HaCaT keratinocyte cell line. This was adressed by using a culture model. The HaCaT cell line (human keratinocytes) was stimulated by MSU (1mg/mL) vs control for 12 hrs. By using genome-wide expression profiling, we identified deregulation of functionally relevant gene networks. HaCaT were obtained from Cell Lines Service (Eppelheim, Germany) and grown in DMEM medium (PAN biotech, Aidenbach, Germany) supplemented with 10% FBS (Life Technology, Grand Island, NY, USA), L-glutamine and non-essential amino acid. Before the treatment HaCaT cells were cultured in serum-free medium for 12hrs. HaCaT were treated with MSU (1mg/ml) vs DMEM control for 12hrs then submitted to RNA extration and gene expression profiling. Triplicate experiments were performed: HaCaT control (n=3), MSU-treated (n=3).
2015-10-29 | E-GEOD-65931 | biostudies-arrayexpress
Project description:The synthetic lethal association between BRCA deficiency and poly (ADP-ribose) polymerase (PARP) inhibition supports PARP inhibitor (PARPi) clinical efficacy in BRCA-mutated tumors. PARPis also demonstrate activity in non-BRCA mutated tumors presumably through induction of PARP1-DNA trapping. Despite pronounced clinical response, therapeutic resistance to PARPis inevitably develops. An abundance of knowledge has been built around resistance mechanisms in BRCA-mutated tumors, however, parallel understanding in non-BRCA mutated settings remains insufficient. In this study, we find a strong correlation between the epithelial-mesenchymal transition (EMT) signature and resistance to a clinical PARPi, Talazoparib, in non-BRCA mutated tumor cells. Genetic profiling demonstrates that SNAI2, a master EMT transcription factor, is transcriptionally induced by Talazoparib treatment or PARP1 depletion and this induction is partially responsible for the emerging resistance. Mechanistically, we find that the PARP1 protein directly binds to SNAI2 gene promoter and suppresses its transcription. Talazoparib treatment or PARP1 depletion lifts PARP1-mediated suppression and increases chromatin accessibility around SNAI2 promoters, thus driving SNAI2 transcription and drug resistance. We also find that depletion of the chromatin remodeler CHD1L suppresses SNAI2 expression and reverts acquired resistance to Talazoparib. The PARP1/CHD1L/SNAI2 transcription axis might be therapeutically targeted to re-sensitize Talazoparib in non-BRCA mutated tumors.
2022-07-08 | PXD033530 | Pride
Project description:The p53 protein is encoded by TP53 gene and plays the key role in significant number of cellular processes including proliferation, apoptosis and regulation of many stress response pathways. P53 acts like a direct transcription activator of numerous genes regulating cell cycle arrest, DNA repair, growth inhibition and many others (Mollereau and Ma, 2014). The canonical biological function of p53 is maintaining genome integrity via elimination of damaged or exposed to genotoxic stress cells. Immortalized HaCaT cells are widely used for keratinocyte research, since they maintain stable keratinocyte phenotype, have nearly unlimited proliferative potential, do not require specific growth and differentiation factors (Colombo et al., 2017). Also, HaCaT cells produce typical differentiation markers such as cytokeratins K14 and K10, involucrin (Colombo et al., 2017) and respond to keratinocyte differentiation stimuli. Taking together, HaCaT cells have similar to normal human keratinocytes (NHK) properties, however, as many of spontaneously immortalized cell lines HaCaT cells bear two mutant p53 alleles - R282Q and H179Y (Lehman et al., 1993). Mutp53 in HaCaT has an increased affinity to other p53 family members (p63, p73), which significantly expands p53 properties. Moreover, mutp53 indirectly affects specific target genes via protein-protein interactions with other transcription factors (NF-Y, E2F1, NF-KB) or by tethering p63 to new promotor locations. For more detailed investigation of mutp53 impact on various processes in HaCaT cells we performed a shRNA mediated knockdown of mutp53. For generation of stable TP53 knockdown we employed plasmid vector pLKO-p53-shRNA-941 (Addgene # #25637) followed by puromycin selection of transduced cells. Here we present proteomic dataset obtained from wild type HaCaT cells and p53 knock down HaCaT keratinocytes.
2022-04-28 | PXD033538 | Pride
Project description:Analyses of the effect of CRISPR/CAS9 mediated knock out of the EMT-transcription factor SNAI2 on the mRNA expression profile of human neuroblastoma SH-SY5Y cells to identify genes that are differentially expressed upon loss of SNAI2. Results provide insight into genes that are repressed by SNAI2 in neuroblastoma cells under normal culture conditions, where loss of SNAI2 enhances the expression of genes involved in biological processes such as neuron development and neuron differentiation.
2020-01-06 | GSE126332 | GEO