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ELF1 expression in prostate cells reduces oncogenic ETS functions and promotes senescence and sensitivity to chemotherapy through distinct gene expression programs

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE113499 | GEO | 2018/07/01

REPOSITORIES: GEO

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ELF1 expression in prostate cells reduces oncogenic ETS functions and promotes senescence and sensitivity to chemotherapy through distinct gene expression programs [RNA-seq]

Project description:Aberrant overexpression of oncogenic ETS factors through chromosomal rearrangments is the most common genomic event in primary prostate tumor and these factors have been well studied. Loss of ELF1, another ETS transcription factor family member, is a common event in prostate cancer, but the function of ELF1 has not been described within the prostate. Studies of ELF1 in different tissue types has determined that it can be important for oncogeneis or tumor suppression. Here, we show that ELF1 is a novel prostate tumor suppressor by hindering oncogenic ETS function at cell migration related genes, but also that ELF1 has the ability to regulate senescence and chemotherapy resistance. Next generation sequencing was used to determine gene expression changes in RWPE-1 cells upon addition of an oncogenic ETS factor and then with the loss of ELF1 through an shRNA knockdown. Genomic binding locations were also determined for ELF1 and ERG, through ChIP-seq to identify any cobound or unique regions. The combination of this data indicates that ELF1 repressed migration related genes which ERG activates, but ELF1 also uniquely binds genes related to cell senescence and activates their transcription. There, these data indicate a novel tumor suppressive mechanism for ELF1 within the prostate and better characterizes its function within this cell type.

2018-07-01 | GSE113485 | GEO

ELF1 expression in prostate cells reduces oncogenic ETS functions and promotes senescence and sensitivity to chemotherapy through distinct gene expression programs [ChIP-seq]

2018-07-01 | GSE113484 | GEO

ELF1 expression in prostate cells reduces oncogenic ETS functions and promotes senescence and sensitivity to chemotherapy through distinct gene expression programs

Project description:ELF1 expression in prostate cells reduces oncogenic ETS functions and promotes senescence and sensitivity to chemotherapy through distinct gene expression programs

| PRJNA451363 | ENA

ELF1 expression in prostate cells reduces oncogenic ETS functions and promotes senescence and sensitivity to chemotherapy through distinct gene expression programs [RNA-seq]

Project description:ELF1 expression in prostate cells reduces oncogenic ETS functions and promotes senescence and sensitivity to chemotherapy through distinct gene expression programs [RNA-seq]

| PRJNA451362 | ENA

ELF1 expression in prostate cells reduces oncogenic ETS functions and promotes senescence and sensitivity to chemotherapy through distinct gene expression programs [ChIP-seq]

Project description:ELF1 expression in prostate cells reduces oncogenic ETS functions and promotes senescence and sensitivity to chemotherapy through distinct gene expression programs [ChIP-seq]

| PRJNA451223 | ENA

Common ELF1 deletion in prostate cancer bolsters oncogenic ETS function, inhibits senescence and promotes docetaxel resistance.

Project description:ETS family transcription factors play major roles in prostate tumorigenesis with some acting as oncogenes and others as tumor suppressors. ETS factors can compete for binding at some cis-regulatory sequences, but display specific binding at others. Therefore, changes in expression of ETS family members during tumorigenesis can have complex, multimodal effects. Here we show that ELF1 was the most commonly down-regulated ETS factor in primary prostate tumors, and expression decreased further in metastatic disease. Genome-wide mapping in cell lines indicated that ELF1 has two distinct tumor suppressive roles mediated by distinct cis-regulatory sequences. First, ELF1 inhibited cell migration and epithelial-mesenchymal transition by interfering with oncogenic ETS functions at ETS/AP-1 cis-regulatory motifs. Second, ELF1 uniquely targeted and activated genes that promote senescence. Furthermore, knockdown of ELF1 increased docetaxel resistance, indicating that the genomic deletions found in metastatic prostate tumors may promote therapeutic resistance through loss of both RB1 and ELF1.

| S-EPMC6305106 | biostudies-literature

The ETS transcription factor ELF1 regulates a broadly antiviral program distinct from the type I interferon response.

Project description:Induction of vast transcriptional programs is a central event of innate host responses to viral infections. Here we report a transcriptional program with potent antiviral activity, driven by E74-like ETS transcription factor 1 (ELF1). Using microscopy to quantify viral infection over time, we found that ELF1 inhibits eight diverse RNA and DNA viruses after multi-cycle replication. Elf1 deficiency results in enhanced susceptibility to influenza A virus infections in mice. ELF1 does not feed-forward to induce interferons, and ELF1's antiviral effect is not abolished by the absence of STAT1 or by inhibition of JAK phosphorylation. Accordingly, comparative expression analyses by RNA-seq revealed that the ELF1 transcriptional program is distinct from interferon signatures. Thus, ELF1 provides an additional layer of the innate host response, independent from the action of type I interferons.

| S-EPMC6932815 | biostudies-literature

Glioblastoma cell populations with distinct oncogenic programs release podoplanin as procoagulant extracellular vesicles.

Project description:Vascular anomalies, including local and peripheral thrombosis, are a hallmark of glioblastoma (GBM) and an aftermath of deregulation of the cancer cell genome and epigenome. Although the molecular effectors of these changes are poorly understood, the upregulation of podoplanin (PDPN) by cancer cells has recently been linked to an increased risk for venous thromboembolism (VTE) in GBM patients. Therefore, regulation of this platelet-activating protein by transforming events in cancer cells is of considerable interest. We used single-cell and bulk transcriptome data mining, as well as cellular and xenograft models in mice, to analyze the nature of cells expressing PDPN, as well as their impact on the activation of the coagulation system and platelets. We report that PDPN is expressed by distinct (mesenchymal) GBM cell subpopulations and downregulated by oncogenic mutations of EGFR and IDH1 genes, along with changes in chromatin modifications (enhancer of zeste homolog 2) and DNA methylation. Glioma cells exteriorize their PDPN and/or tissue factor (TF) as cargo of exosome-like extracellular vesicles (EVs) shed from cells in vitro and in vivo. Injection of glioma-derived podoplanin carrying extracelluar vesicles (PDPN-EVs) activates platelets, whereas tissue factor carrying extracellular vesicles (TF-EVs) activate the clotting cascade. Similarly, an increase in platelet activation (platelet factor 4) or coagulation (D-dimer) markers occurs in mice harboring the corresponding glioma xenografts expressing PDPN or TF, respectively. Coexpression of PDPN and TF by GBM cells cooperatively affects tumor microthrombosis. Thus, in GBM, distinct cellular subsets drive multiple facets of cancer-associated thrombosis and may represent targets for phenotype- and cell type-based diagnosis and antithrombotic intervention.

| S-EPMC7993100 | biostudies-literature

The ETS transcription factor ELF1 regulates a critical, broadly antiviral program distinct from the type I interferon response

Project description:Induction of vast transcriptional programs is a central event of innate host responses to viral infections. Here we report a unique transcriptional program with potent antiviral activity, driven by E74-like ETS transcription factor 1 (ELF1). Using high-content microscopy to quantify viral infection over time, we found that ELF1 inhibits eight diverse RNA and DNA viruses uniquely at multi-cycle replication. Elf1 deficiency results in enhanced susceptibility to influenza A virus infections in mice. ELF1 does not feed-forward to induce interferons, and ELF1’s antiviral effect is not abolished by the absence of STAT1 or by inhibition of JAK phosphorylation. Accordingly, comparative expression analyses by RNAseq revealed that the ELF1 transcriptional program is distinct from interferon signatures. Thus, ELF1 provides an additional layer of the innate host response, independent from the action of type I interferons.

2019-10-24 | GSE136864 | GEO

The ETS transcription factor ELF1 regulates a critical, broadly antiviral program distinct from the type I interferon response

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-10-24 | GSE122252 | GEO