Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA246033 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In order to identify the p53-independent program controlled by E4F1, we performed microarray analyses in p53 KO and p53 KO; Ha-RasV12-transformed mouse embryonic fibroblasts (MEFs) in wild type and E4F1-inactivated cells. To address p53-independent E4F1 transcriptome, a 12 chip array study has been realized using total RNA recovered from wild-type (E4F1+/flox, CRE infected; odd Samples) MEFs and E4F1-depleted (E4F1-/flox, CRE infected; even Samples) MEFs in p53-/- (Samples 1 to 12) and p53-/-, Ha-RasV12 background (Samples 13 to 24). p53-/- MEFs were derived from 13.5-day mouse embryos. Transformed p53-/- MEFs were generated by infection with a recombinant retrovirus encoding for Ha-RasV12. Three independent biological replicates of wild-type and knock-out MEFs for E4F1 have been used on the two genetic backgrounds.
2015-04-01 | E-GEOD-57240 | biostudies-arrayexpress
Project description:E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In order to identify the p53-independent program controlled by E4F1, we performed microarray analyses in p53 KO and p53 KO; Ha-RasV12-transformed mouse embryonic fibroblasts (MEFs) in wild type and E4F1-inactivated cells.
2015-04-01 | GSE57240 | GEO
Project description:ChIP-seq of E4F1 in primary mouse embryonic fibroblasts (MEFs) and in p53-/-, Ha-RasV12-transformed MEFs
| PRJNA246035 | ENA
Project description:E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In order to decipher E4F1 cellular target genes, we performed chromatin immunoprecipitation of endogenous E4F1 in primary and in p53KO, Ha-RasV12-transformed MEFs. Both input and immunoprecipitated DNA were exhaustively sequenced and mapped on the mouse genome (mm9). Peak detection has been achieved by combining two peak calling algorithms. Intersection of the two E4F1 peak lists on each cell line were considered as E4F1 chromatin bound regions. Genome-wide mapping of E4F1 binding in mouse embryonic fibroblasts.
2015-04-01 | E-GEOD-57228 | biostudies-arrayexpress
Project description:E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In order to decipher E4F1 cellular target genes, we performed chromatin immunoprecipitation of endogenous E4F1 in primary and in p53KO, Ha-RasV12-transformed MEFs. Both input and immunoprecipitated DNA were exhaustively sequenced and mapped on the mouse genome (mm9). Peak detection has been achieved by combining two peak calling algorithms. Intersection of the two E4F1 peak lists on each cell line were considered as E4F1 chromatin bound regions.
2015-04-01 | GSE57228 | GEO
Project description:Oncogenic stress-induced senescence initially inhibits tumor initiation by blocking proliferation. If these cells are not eliminated they may resume proliferation upon loss-of-tumor suppressors, and be at risk of transformation. During tumor formation, depending on the sequence of events of gain-of-oncogenes and/or loss-of-tumor suppressors, cancer cells may emerge from senescent cells. The goal of this study is to determine if transformed cells after senescence (TS) display more aggressive tumorigenic features, with a greater capacity to migrate and a higher resistance to anti-tumoral drugs than cells having undergone transformation without senescence. Here, we modeled cell transformation using mouse embryonic fibroblasts (MEFs) subjected to an inverse sequence of events: i) gain-of-RasV12 oncogene and loss-of-p53 tumor suppressor, leading to transformed cells after senescence (TS), or ii) the opposite, resulting in transformed (T) non-senescent cells.
2022-07-30 | GSE210060 | GEO
Project description:Newly emerging transformed cells carrying genetic defects, including the active Ras mutant, are apicall extruded when surrounded by normal epithelial cells. This biological phenomenon is termed as cell competition. It remains elusive which factors prime RasV12-transformed cells to be expelled via cell competition. Here, We performe microarray analysis to search for molecules whose expression is changed in RasV12 cells surrounded by normal cells.
2023-07-11 | GSE236658 | GEO
Project description:The activation of different oncogenic signals may primarily contribute to the heterogeneity of cancer cells. However, the exact mechanisms underlying different oncogenic transformation are still unclear. We used the c-Myc, H-Ras and Akt transformed liver cell model to define mRNA expression profiles in the non-transformed and the three types of oncogene-transformed cells Purified p53-/- mouse fetal liver progenitor cells were transformed by three oncogenic genetic factors, c-Myc, H-RasV12 and myristoylated-AKT1(myr-Akt). The gene expression profilings of transformed cells and control cells were analyzed through microarray.
2013-02-02 | E-GEOD-43991 | biostudies-arrayexpress
Project description:We engineered KSR1-/- mouse embryonic fibroblasts (MEFs) to express GFP alone, KSR1 or RasV12 and GFP, or KSR1, H-RasV12 and GFP, and performed gene expression profiling on all 4 cell lines.
2011-04-02 | GSE28228 | GEO
Project description:Normal epithelial cells exert their competitive advantage over RasV12-transformed cells and eliminate them into apical lumen via cell competition. However, it remains elusive which internal or external factors compromise cell competition and provoke oncogenesis. Here, we examine the effect of sequential accumulation of gene mutations mimicking multi-sequential carcinogenesis on RasV12-induced cell competition. Consequently, we find that directionality of cell extrusion of RasV12 cells mosaically produced within Wnt-activated epithelia is reversed, and transformed cells are delaminated into basal lamina via non-cell autonomous MMP21 upregulation. Elevated production of MMP21 is elicited partly through NF-κB signaling, which blockage restores apical elimination of RasV12 cells. Collectively, this study demonstrates that cells with high mutational burdens exploit cell competition for their benefit by behaving as unfit cells and are endowed with an invasion advantage. We performed microarray analysis to search for molecules whose expression is changed in β-catenin Δ131/RasV12 cells surrounded by β-catenin Δ131 cells.
2022-11-16 | GSE217830 | GEO