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Transcriptional profiles LPC-HRas cells with or without ETV4 knockdown

ABSTRACT: Transcriptional profiles LPC-HRas cells with or without ETV4 knockdown

PROVIDER: PRJNA765637 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16025537_1.fastq.gz	Fastqsanger.gz
	SRR16025537_2.fastq.gz	Fastqsanger.gz
	SRR16025538_1.fastq.gz	Fastqsanger.gz
	SRR16025538_2.fastq.gz	Fastqsanger.gz

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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

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Project description:To investigate the gene expression changes due to LPC-induced calcific nodule formation in porcine aortic valve interstitial cells (paVICs). We then examined differential gene expression due to treatment with dantrolene, which inhibits calcific nodule formation, with and without LPC after 24 hours of exposure.

2023-03-30 | GSE227229 | GEO

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

Gene expression changes upon knockdown or over-expression of the ETS gene ETV4 in prostate cancer cell lines

Project description:Chromosomal abnormalities that give rise to elevated expression levels of the ETS genes ETV1, ETV4, ETV5, or ERG are prevalent in prostate cancer, but the function of these transcription factors in carcinogenesis is not clear. Previous work implicates ERG, ETV1, and ETV5 as regulators of invasive growth but not transformation in cell lines. Here we show that the PC3 prostate cancer cell line provides a model system to study the over-expression of ETV4. Anchorage independent growth assays and microarray analysis indicate that high ETV4 expression is critical for the transformation phenotype of PC3 cells. However, genes up-regulated upon ETV4 over-expression were very similar to genes up-regulated by ETV1 over-expression in the RWPE-1 normal prostate cell line. Together these data indicate that the ETV4 dependent transformation phenotype observed in PC3 cells is due to the genetic background of the cell line, rather than a distinct characteristic of ETV4. Furthermore, these findings suggest that the function of ETS genes in prostate cancer may differ based on other genetic alterations in a tumor. Two sets of two color experiments. First is PC3 cells expressing one of two independent ETV4 shRNAs versus PC3 cells expressing a control shRNA (luciferase). Second is RWPE-1 cells expressing 3xFlag tagged ETV4 versus RWPE-1 cells with a control (empty) vector.

2011-03-24 | E-GEOD-21209 | biostudies-arrayexpress

RNASeq to investigate ETV4 and ETV5 function in human foetal lung tip progenitor cells

Project description:In order to understand transcription factor ETV4 and ETV5 function, we have knocked down ETV4 and ETV5 synergistically in human foetal lung tip progenitor organoids using an inducible CRISPRi system. We discovered that ETV double knockdown led to organoid cell self-renewal defects

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Identification of ETV4-responsive genes in NSCLC cells

Project description:H1703, H1299, and H358T cells treated with or without si-ETV4 were used to screen the global profiling of human long-noncoding RNAs (lncRNAs) and protein-coding transcripts.

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Gene expression of wild-type and Ppar-beta null primary keratinocytes, with and without infection with an activated Hras retrovirus, with and without the Ppar-beta specific ligand GW0742

Project description:Differential gene expression profiles were observed in response to Hras in either wild-type or Ppar-beta null primary keratinocytes and differentail gene edxpression profiles by GW0742 were only found in wild-type keratinocytes. Primary keratinocytes from wild-type and Ppar-beta null mice were either mock infected or infected with an Hras encoding retrovirus and treated with or without 1 uM GW0742 for 24 hours.

2012-04-11 | E-GEOD-32498 | biostudies-arrayexpress

Normal mouse skin lacking Hras

2015-03-01 | GSE60769 | GEO

Normal mouse skin lacking Hras

Project description:Oncogenic activating mutations in Ras genes are among the most common drivers of human disease. Treating mouse skin with the chemical carcinogen DMBA induces a characteristic mutation in Hras at codon 61. To understand how skin responds to a constitutive lack of Hras, we generated a cohort of Hras knockout mice. A backcross was generated using male Mus spretus and female FVB/N Hras-/- mice; female F1 hybrids were mated with male FVB/N Hras -/- or Hras -/+ mice to generate a backcross population. This series contains mice that were Hras -/-. Mice were aged to 8 weeks and a tail skin sample was snap frozen.

2015-03-01 | E-GEOD-60769 | biostudies-arrayexpress

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.

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