DNase-seq during MCF10A-ER-Src cell transformation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE100255 | GEO | 2017/07/03
SECONDARY ACCESSION(S): PRJNA391165
REPOSITORIES: GEO
Similar Datasets
Project description:We performed ChIP-seq for histone modifications to map chromatin status and dynamics during MCF10A-ER-Src cell transformation.
2017-07-03 | GSE100257 | GEO
Project description:We performed RNA-seq to examine RNA expression profiles during MCF10A-ER-Src cell transformation and upon knockdowns of transcription factors
2017-07-03 | GSE100258 | GEO
Project description:We applied ribosome profiling and RNA sequencing to examine gene expression regulation during oncogenic cell transformation. One model involves normal mammary epithelial cells (MCF10A) containing ER-Src. Treatment of such cells with tamoxifen rapidly induces Src, thereby making it possible to kinetically follow the transition between normal and transformed cells. The other model consists of three isogenic cell lines derived from primary fibroblasts in a serial manner (Hahn et al., 1999). EH cell is immortalized by overexpression of telomerase (hTERT), and exhibits normal fibroblast morphology. EL cell expresses hTERT along with both large and small T antigens of Simian virus 40, and it displays an altered morphology but is not transformed. ELR cell expresses hTERT, T antigens, and an oncogenic derivative of Ras (H-RasV12).
2015-11-13 | GSE65885 | GEO
Project description:siSTAT3 knockdown of a tamoxifen initiated, transformation inducible, breast cancer model system (MCF10A-ER-Src), with associated controls of EtOH and siNEG treatments. A description of MCF10A-ER-Src cells can be found here: www.encodeproject.org
2015-06-01 | GSE64536 | GEO
Project description:DNase-seq during MCF10A-ER-Src cell transformation
| PRJNA391165 | ENA
Project description:To address the molecular mechanisms underlying c-Src-mediated tumor progression, we previously developed a model system using Csk-deficient fibroblasts that can be transformed by wild-type c-Src. In this study, we applied this system for the analysis of the potential contribution of miRNA to c-Src-mediated transformation. Pair-wise significance analysis of the microarray indicated that seven miR genes were significantly upregulated and six miRNA genes were downregulated in c-Src-transformed cells with a P value below 0.01 and with a fold change over 2.0. Csk-/- mouse embryonic fibroblasts (Csk-/- MEFs) were transfected with empty vector, c-Src, Csk/c-Src, or Csk. Each sample was run in duplicate.
2011-02-17 | E-GEOD-23426 | biostudies-arrayexpress
Project description:Despite significant progress, our understanding of how specific oncogenes transform cells is still limited and likely underestimates the complexity of downstream signalling events. Herein, we describe a novel, integrated approach that addresses this knowledge gap. This utilizes mass spectrometry-based chemical proteomics to characterize the global impact of an oncogene on the expressed kinome, and then functionally annotates the regulated kinases. As an example, we identified approximately seventy protein kinases exhibiting altered expression and/or phosphorylation in Src-transformed mammary epithelial cells. An integrated siRNA screen identified nine kinases, including SGK1, as being essential for Src-induced transformation. In triple negative breast cancer cells, which exhibit a prominent signalling network governed by src family kinases, Src positively regulated SGK1 expression and combined inhibition of Src and SGK1 was more effective at inhibiting colony formation in vitro, and xenograft growth in vivo, than either treatment alone. Therefore, this approach not only provides major mechanistic insights into oncogenic transformation but also aids the design of improved therapeutic strategies.
2019-01-14 | PXD010687 | Pride
Project description:We reported that stable expression of constitutively active intra cellular Notch (ICN), in quail neuroretina (QNR) cells transformed by a conditional v-Src mutant (QNR/v-src cells), resulted in the suppression of their transformed properties. Acquisition of a normal phenotype coincided with a major switch in cell identity, as these undifferentiated QNR/v-src cells acquired characteristics of glial differentiation. Similar loss of transformation and gene reprogramming can be achieved in QNR/v-src cells, stably expressing the human CBF protein, RBP-Jk, whose activity was rendered ligand independent by fusion to the VP16 transactivator. These major phenotypic changed are correlated with a dominant interference with signaling effectors, regulating cell morphology and cytoskeleton organization. To understand the mechanisms by which Notch signaling activation suppressed v-Src induced cell transformation and induced differentiation, we compared the transcription profile of QNR cells transformed by a v-Src mutant encoding a temperature sensitive oncoprotein (QNR/v-src), with that of cells stably expressing ICN (QNR/v-src/ICN) or RBP-Jk-VP16 (QNR/v-src/RBP-Jk-VP16). Total RNA was extracted from QNR/v-src, QNR/v-src/ICN or QNR/v-src/RBP-Jk-VP16 cells maintained at permissive (37°C) or restrictive (41°C) temperature. cDNA from QNR/v-src cells was probed with that of QNR/v-src/ICN or QNR/v-src/RBP-Jk-VP16 at both temperature on microarrays spotted with 13,000 cDNA from chicken EST collections designed by the genomic facility of the Fred Hutchinson Cancer Research Center (Seattle). For two sets of sample, dye swap experiments were performed.
2010-12-01 | E-GEOD-22054 | biostudies-arrayexpress
Project description:To address the molecular mechanisms underlying c-Src-mediated tumor progression, we previously developed a model system using Csk-deficient fibroblasts that can be transformed by wild-type c-Src. In this study, we applied this system for the analysis of the potential contribution of miRNA to c-Src-mediated transformation. Pair-wise significance analysis of the microarray indicated that seven miR genes were significantly upregulated and six miRNA genes were downregulated in c-Src-transformed cells with a P value below 0.01 and with a fold change over 2.0.
2011-02-17 | GSE23426 | GEO
Project description:We reported that stable expression of constitutively active intra cellular Notch (ICN), in quail neuroretina (QNR) cells transformed by a conditional v-Src mutant (QNR/v-src cells), resulted in the suppression of their transformed properties. Acquisition of a normal phenotype coincided with a major switch in cell identity, as these undifferentiated QNR/v-src cells acquired characteristics of glial differentiation. Similar loss of transformation and gene reprogramming can be achieved in QNR/v-src cells, stably expressing the human CBF protein, RBP-Jk, whose activity was rendered ligand independent by fusion to the VP16 transactivator. These major phenotypic changed are correlated with a dominant interference with signaling effectors, regulating cell morphology and cytoskeleton organization. To understand the mechanisms by which Notch signaling activation suppressed v-Src induced cell transformation and induced differentiation, we compared the transcription profile of QNR cells transformed by a v-Src mutant encoding a temperature sensitive oncoprotein (QNR/v-src), with that of cells stably expressing ICN (QNR/v-src/ICN) or RBP-Jk-VP16 (QNR/v-src/RBP-Jk-VP16).
2010-12-01 | GSE22054 | GEO