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ERG induced mesenchymal like gene signature

ABSTRACT: ERG overexpression was conducted in stably transfected K562 cell line with a tet-on inducible plasmid habouring ERG3. Prolonged induction of ERG (8 days) produced spindle cell shape changes whereas non-induced cells retained the round morphology. In oder to determine the genes responsible for inducing cell shape changes, a genome wide transcriptional screen was conducted.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51258 | GEO | 2013/10/19

SECONDARY ACCESSION(S): PRJNA222990

REPOSITORIES: GEO

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ERG induced mesenchymal like gene signature

Project description:ERG overexpression was conducted in stably transfected K562 cell line with a tet-on inducible plasmid habouring ERG3. Prolonged induction of ERG (8 days) produced spindle cell shape changes whereas non-induced cells retained the round morphology. In oder to determine the genes responsible for inducing cell shape changes, a genome wide transcriptional screen was conducted. Three clones that potently induced ERG overexpression (8 days) with the corresponding non-induced cells were hybridized.

2013-10-19 | E-GEOD-51258 | biostudies-arrayexpress

Genome wide screen reveals WNT11, a noncanonical WNT gene, as a target of ETS transcription factor ERG

Project description:ERG is a transcription factor that is involved in leukomogenesis and its mRNA overexpression has been associated with poor prognosis in a subset of patients with T-cell acute lymphoblastic leukemia (T-ALL) and acute myeloid leukemia (AML). Herein, a genome-wide screen of ERG target genes was conducted by chromatin immunoprecipitation-on-chip (ChIP-chip) in Jurkat cells. 342 significant annotated regions were derived from ChIP-chip experiments. Seventeen candidate promoter regions resulted in at least two-fold enrichment by quantitative PCR. Notably, ERG potential targets included WNT signaling genes: WNT2, WNT9A, WNT11, CCND1, and FZD7. Functionally, expression of WNT11 was downregulated with siRNA ERG knockdown and substantially upregulated in a tet-on ERG-inducible assay in K562 cells. To investigate a role for ERG in WNT signaling, a WNT agonist was used to inhibit glycogen synthase kinase (GSK-3). This treatment resulted in an ERG-dependent proliferative growth advantage in the tet-on ERG-inducible system. Lastly, chromatin immunoprecipitation assays of primary leukemia blasts confirmed WNT11 promoter enrichment dependent on ERG mRNA expression. In conclusion, ERG transcriptional networks in leukemia are revealed. Specifically, WNT11 emerged as a target of ERG. We propose that overexpression of ERG in acute leukemia may lead to a proliferative advantage upon activation of WNT signals.

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Genome wide screen reveals WNT11, a noncanonical WNT gene, as a target of ETS transcription factor ERG

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TMPRSS2:ERG promotes invasiveness and epithelial to mesenchymal transition in prostate cancer model

Project description:Recently, a frequent chromosomal aberration fusing Androgen regulated TMPRSS2 promoter and the ERG gene (T/ERG) was discovered in prostate cancer. Several studies demonstrated cooperation between the T/ERG and other defective pathways in cancer progression however, the biological mechanism by which the T/ERG operates is yet to be determined. Using immortalized prostate epithelial cells (EP) model we were able to show that EP with the combination of androgen receptor(AR) and T/ERG(EP-AR T/ERG cell line) demonstrate an Epithelial to Mesenchymal Transition (EMT) manifested by a mesenchyme-like morphological appearance and behavior. To further elucidate the mechanism by which T/ERG executes the EMT program at large, we took a genome-wide approach and conducted micro-array based comparison between EP-AR and EP-AR T/ERG cells

2010-12-30 | GSE22010 | GEO

The transcriptional network of wild type ERG and ERG mutant at K362

Project description:We have identified a specific site in the ERG protein that undergoes post-transcriptional modification. We have mutated this site and generated stably expressing LNCaP cell lines. In this study we evaluated the transcriptional profile induced by ERG in LNCaP stably expressing ERG wild type , ERG mutant or empty vector (EV).

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TMPRSS2:ERG promotes invasiveness and epithelial to mesenchymal transition in prostate cancer model

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ERG activity is regulated by endothelial FAK coupling with TRIM25/USP9x in vascular patterning

Project description:Precise vascular patterning is critical for normal growth and development. The ERG transcription factor drives Delta like ligand 4 (DLL4)/Notch signalling and is thought to act as pivotal regulators of endothelial cell (EC) dynamics and developmental angiogenesis. However, molecular regulation of ERG activity remains obscure. Using a series of EC specific Focal Adhesion Kinase (FAK)-knockout (KO) and point-mutant FAK-knockin mice, we show that loss of ECFAK, its kinase activity or phosphorylation at FAK-Y397, but not FAK-Y861, reduces ERG and DLL4 expression levels together with concomitant aberrations in vascular patterning. Rapid Immunoprecipitation Mass Spectrometry of Endogenous Proteins identified that endothelial nuclear-FAK interacts with the de-ubiquitinase USP9x and the ubiquitin ligase TRIM25 enzymes. Further in silico analysis corroborates that ERG interacts with USP9x and TRIM25. Moreover, ERG levels are reduced in FAKKO ECs via a ubiquitin-mediated post-translational modification programme involving USP9x and TRIM25. Re-expression of ERG in vivo and in vitro rescues the aberrant vessel sprouting defects observed in the absence of ECFAK. Our findings identify ECFAK as a regulator of retinal vascular patterning by controlling ERG protein degradation via TRIM25/USP9x.

2022-07-05 | PXD033447 | Pride

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Project description:This dataset contains rawRNA-seq data from HFL-1 Cells Overexpressed GFP, GFP-ERG or GFP-ERG-ΔIDR13. The experiment aims to explore the downstream genes of ERG and its phase separation-deficient mutant to uncover the role of ERG's LLPS activity in regulating gene expression in HFL-1 cells, providing insights into the regulatory networks controlled by ERG in cell senescence.

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ERG-mediated coregulator complex formation maintains androgen receptor signaling in prostate cancer [ERG ChIP]

Project description:We report the effects of ERG on prostate tumorigenesis, ERG-mediated oncogene addiction, and downstream AR signaling pathways. We determined that ERG facilitates AR-signaling and mediates transformation of prostate cells by maintaining coregulator complex formation at AR-bound sites across the genome.

2020-09-04 | GSE157406 | GEO

ERG-Proximity biotin labeling_2022-03-30

Project description:ERG N-terminal FLag-BirA* fusion, BioID performed in T-REx Flp-In HEK923.

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