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Aberrant stabilized ETV4 expression cooperates with loss of p53 to promote invasive prostate carcinoma

ABSTRACT: Aberrant stabilized ETV4 expression cooperates with loss of p53 to promote invasive prostate carcinoma

PROVIDER: PRJNA535484 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8955990_1.fastq.gz	Fastqsanger.gz
	SRR8955990_2.fastq.gz	Fastqsanger.gz
	SRR8956000.fastq.gz	Fastqsanger.gz
	SRR8955991_1.fastq.gz	Fastqsanger.gz
	SRR8955991_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Aberrant stabilized ETV4 expression cooperates with loss of p53 to promote invasive prostate carcinoma

Project description:Chromosomal translocations or upregulations involving ETS transcription factor are frequent events in prostate cancer pathogenesis and significantly co-occurrence with p53 or PTEN loss. Caused by the low stabilities of ETS proteins in cytosol, mouse models with aberrant expression of wild type ETS transcription factors had subtle phenotypes and only drive prostate cancer progression in the setting of Pten loss. Here we show that prostate specific aberrant expression of mutated ETV4 (V70P71D72-AAA, ETV4-AAA), which is resistence to COP1 mediated protein degradation, results in more stabilized ETV4 protein in mouse prostate. We found that ETV4-AAA mice develop marked prostatic intraepithelial neoplasia (mPin) and p53-dependent cell senescence within 2 weeks, but without tumor development when aged. Interestingly, ETV4-AAA positive cells reduce dramatically in a PTEN loss background, which means that there is no cooperation between ETV4-AAA and PTEN loss. Aberrant ETV4-AAA expression promotes progression of mPin to prostatic adenocarcinoma in a Tp53 deficiency or haploinsufficiency background. In contrast to PTEN loss induced mouse prostate cancers which loss NKX3.1 expression and resistant to castration therapy, these ETV4-AAA tumor cells well maintain AR and NKX3.1 expression and are sensitive to castration therapy.

2021-01-01 | GSE130311 | GEO

ETV4 mediates dosage-dependent prostate tumor initiation and cooperates with p53 loss to generate prostate cancer.

Project description:Comparision of transcriptome of PC3 and 22Rv1 prostate cell lines after 1 week overexpression of mutated ETV4: ETV4AAA-IRES-eGFP, wild type ETV4: ETV4WT-IRES-eGFP, and control vector IRES-eGFP by MSCV-IRES-GFP vector ((Addgene #20672)) and Lentivirus transduction.

2022-10-16 | GSE215437 | GEO

ETV4 mediates dosage-dependent prostate tumor initiation and cooperates with p53 loss to generate prostate cancer

Project description:ETV4 mediates dosage-dependent prostate tumor initiation and cooperates with p53 loss to generate prostate cancer

| PRJNA833855 | ENA

ETV4 mediates dosage-dependent prostate tumor initiation and cooperates with p53 loss to generate prostate cancer.

Project description:ETV4 mediates dosage-dependent prostate tumor initiation and cooperates with p53 loss to generate prostate cancer.

| PRJNA890267 | ENA

Mutant p53 cooperates with ETS2 to promote etoposide resistance

Project description:This SuperSeries is composed of the following subset Series: GSE36749: Mutant p53 cooperates with ETS2 to promote etoposide resistance [ChIP-Seq] GSE36751: Mutant p53 cooperates with ETS2 to promote etoposide resistance [ChIP-chip] Refer to individual Series

2012-05-02 | E-GEOD-36752 | biostudies-arrayexpress

Murine ES Cells: Control vs. ETV4/5 double KO

Project description:ETS-related transcription factors ETV4 and ETV5 play crucial roles for organogenesis and morphogenesis. We compared the transcriptional profiles between wild-type and ETV4 and ETV5 double knockout (ETV4/5 dKO) ES cells by an oligo DNA microarray analysis. Self-renewal capacity and pluripotency are known to be controlled by an ES cell-specific transcription factor network; therefore, we focused on transcription-associated genes. Of 1258 transcription-related genes, 47 genes were significantly downregulated and 98 genes were significantly upregulated in ETV4/5 dKO ES cells. Several genes whose expression is specific to undifferentiated ES were repressed in ETV4/5 dKO ES cells. In contrast, expression of differentiation markers was enhanced in ETV4/5 dKO ES cells.

2015-09-13 | GSE47225 | GEO

ETV4 mediates dosage-dependent prostate tumor initiation and cooperates with p53 loss to generate prostate cancer.

Project description:The mechanisms underlying ETS-driven prostate cancer initiation and progression remain poorly understood due to a lack of model systems that recapitulate this phenotype. We generated a genetically engineered mouse with prostate-specific expression of the ETS factor, ETV4, at lower and higher protein dosage through mutation of its degron. Lower-level expression of ETV4 caused mild luminal cell expansion without histologic abnormalities, and higher-level expression of stabilized ETV4 caused prostatic intraepithelial neoplasia (mPIN) with 100% penetrance within 1 week. Tumor progression was limited by p53-mediated senescence and Trp53 deletion cooperated with stabilized ETV4. The neoplastic cells expressed differentiation markers such as Nkx3.1 recapitulating luminal gene expression features of untreated human prostate cancer. Single-cell and bulk RNA sequencing showed that stabilized ETV4 induced a previously unidentified luminal-derived expression cluster with signatures of cell cycle, senescence, and epithelial-to-mesenchymal transition. These data suggest that ETS overexpression alone, at sufficient dosage, can initiate prostate neoplasia.

| S-EPMC10075989 | biostudies-literature

shRNA-mediated knockdown of ETV4 and MED25 in the prostate cell line PC3 reveals set of genes potentially coregulated by MED25 and ETV4

Project description:Our in vitro binding studies support a model whereby MED25 exhibits multivalent interactions with a subset of related ETS factors, ETV1/4/5. We hypothesize that the interaction would allow for coregulation of genes by ETV1/4/5 and MED25, acting perhaps to link the ETVs to the Mediator complex. To explore this possibility, we compared the genome occupancy for FLAG-tagged MED25 and ETV4 in the prostate cancer cell line PC3, which overexpresses ETV4. We also tested for relevance of MED25 and ETV4 binding to for gene expression in PC3s. We found a high degree of overlap in the FLAG-MED25 and ETV4 ChIPs datasets consistent with our model, and also identified a subset of target genes co-dependent on Med25 and ETV4.

2019-06-28 | GSE133447 | GEO

Transcriptional profiles LPC-HRas cells with or without ETV4 knockdown

Project description:To determine the molecular signaling pathways responsible for ETV4 regulation of cell growth, RNA sequencing was conducted on LPC-HRas cells with or without ETV4 knockdown

2021-10-30 | GSE184680 | GEO

Spatiotemporal lineage derepression by cell crowding-induced ETV4 inactivation

Project description:All extant amniotes employ a single-layered epithelium of epiblasts as a starting material for gastrulation, suggesting the necessity of the epithelial structure for three germ layer derivation. Using a human embryonic stem cell (hESC) epithelium as a model system, we found that local epithelial crowding derepresses the neuroectoderm fate by spatiotemporal inactivation of ETV4. ETV4 serves as a genetic toggle switch that links cell density to lineage fates. Mechanistically, cell crowding blocks FGF receptor endocytosis by reduced cell-extracellular matrix (ECM) interaction. Disrupted endocytosis decreases ETV4 protein stability by ERK inactivation. Mathematical modeling of epithelial crowding demonstrates that the cooperativity of integrin-ECM interaction transforms the gradient of crowdedness into bistable ETV4 transition, which ensures the switch-like function of ETV4 in lineage determination. Our results propose local cell crowding in a stem cell epithelium as a key cellular mechanism for spatiotemporal regulation of lineage fates.

2024-03-12 | GSE183702 | GEO

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