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The self-renewal function of Oct-4 can be replaced by the EWS-OCT-4 fusion protein in embryonic stem cells

ABSTRACT: The self-renewal function of Oct-4 can be replaced by the EWS-OCT-4 fusion protein in embryonic stem cells

PROVIDER: PRJNA1243900 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32912409_1.fastq.gz	Fastqsanger.gz
	SRR32912409_2.fastq.gz	Fastqsanger.gz
	SRR32912410_1.fastq.gz	Fastqsanger.gz
	SRR32912410_2.fastq.gz	Fastqsanger.gz
	SRR32912411_1.fastq.gz	Fastqsanger.gz

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The self-renewal function of Oct-4 can be replaced by the EWS-OCT-4 fusion protein in embryonic stem cells

Project description:EWS-Oct-4 can effectively replace Oct-4, which has significant implications for advancements in stem cell research and regenerative medicine

2025-04-02 | GSE293283 | GEO

FGF4 is a target of EWS-OCT-4 in Embryonic stem cell

Project description:FGF4 has key role in self-renewal and differentiation of Embryonic stem cell, and Fgf4 is activated by direct binding of ESW-OCT-4 through its enhancer

2018-08-08 | GSE118212 | GEO

Fusion protein EWS-FLI1 is incorporated into a protein granule in cells

Project description:Ewing sarcoma is driven by fusion proteins containing a low complexity (LC) domain that is intrinsically disordered and a powerful transcriptional regulator. The most common fusion protein found in Ewing sarcoma, EWS-FLI1, takes its LC domain from the RNA-binding protein EWSR1 (Ewing Sarcoma RNA-binding protein 1) and a DNA-binding domain from the transcription factor FLI1 (Friend Leukemia Virus Integration 1). The LC domain in EWS-FLI1 can bind RNA polymerase II (RNA Pol II) and can self-assemble through a process known as phase separation. The ability of EWSR1 and related RNA-binding proteins to assemble into ribonucleoprotein granules in cells has been intensely studied but the role of phase separation in EWS-FLI1 activity is less understood. We investigated the overlapping functions of EWSR1 and EWS-FLI1 in controlling gene expression and tumorigenic cell growth in Ewing sarcoma, and our results suggested that these proteins function closely together. We then studied the nature of interactions among EWS-FLI1, EWSR1, and RNA Pol II. We observed EWSR1 and RNA Pol II to be present in protein granules in cells. We then identified protein granules in cells associated with the fusion protein, EWS-FLI1. The tyrosine residues in the LC domain are required for the abilities of EWS-FLI1 to bind its partners, EWSR1 and RNA Pol II, and to incorporate into protein granules. These data suggest that interactions among EWS-FLI1, RNA Pol II, and EWSR1 in Ewing sarcoma can occur in the context of a molecular scaffold found within protein granules in the cell.

2020-07-23 | GSE154944 | GEO

REPLACED BY GSE136256

Project description:REPLACED BY GSE136256

| PRJNA415907 | ENA

Rewiring the fusion oncoprotein EWS/FLI1 in Ewing sarcoma with bivalent small molecules [RNA-seq]

Project description:Deregulated transcription is a defining hallmark of cancer, especially pediatric malignancies, which are frequently driven by fusion transcription factors. Targeting transcription factors directly has been challenging as they lack druggable pockets. Recently, chemically induced proximity has enabled the rewiring of transcriptional activators to drive expression of pro-apoptotic genes using bivalent small molecules. Targeting fusion transcription factors, such as EWS/FLI in Ewing sarcoma, with these compounds, may open new therapeutic venues. Here, we develop a small molecule, EB-TCIP, that recruits FKBP12F36V-tagged EWS/FLI1 to DNA sites bound by the transcriptional regulator BCL6, leading to rapid and sustained expression of BCL6 target genes. EB-TCIP activity is dependent on ternary complex formation and specific to cells that express FKBP-EWS/FLI1. This proof-of-concept study demonstrates that EWS/FLI1 can be relocalized on chromatin to induce genes that are ordinarily regulated by a transcriptional repressor. Insights herein will guide the development of bivalent molecules for fusion transcription factors.

2025-03-17 | GSE290895 | GEO

Rewiring the fusion oncoprotein EWS/FLI1 in Ewing sarcoma with bivalent small molecules [ChIP-seq]

2025-03-17 | GSE290894 | GEO

Rewiring the fusion oncoprotein EWS/FLI1 in Ewing sarcoma with bivalent small molecules [ATAC-seq]

2025-03-17 | GSE290893 | GEO

FGF4 is a target of EWS-OCT-4 in Embryonic stem cell

Project description:FGF4 is a target of EWS-OCT-4 in Embryonic stem cell

| PRJNA484876 | ENA

Cell-type dependent enhancer binding of the EWS/ATF1 fusion gene in clear cell sarcomas

Project description:Clear cell sarcoma (CCS) is a rare soft tissue sarcoma caused by the EWS/ATF1 fusion gene. Here, we established induced pluripotent stem cells (iPSCs) from EWS/ATF1-controllable murine CCS cells harboring sarcoma-associated genetic abnormalities. Sarcoma-iPSC mice develop secondary sarcomas immediately after EWS/ATF1 induction, but only in soft tissue. EWS/ATF1 expression induces oncogene-induced senescence in most cell types in sarcoma-iPSC mice but prevents it in sarcoma cells. We identify Tppp3-expressing cells in peripheral nerves as a cell-of-origin for these sarcomas. We show cell type-specific recruitment of EWS/ATF1 to enhancer regions in CCS cells. Finally, epigenetic silencing at these enhancers induces senescence and inhibits CCS cell growth through altered EWS/ATF1 binding. Together, we propose that distinct responses to premature senescence are the basis for the cell type-specificity of cancer development.

2019-07-18 | GSE77204 | GEO

Cell-type dependent enhancer binding of the EWS/ATF1 fusion gene in clear cell sarcomas

2019-07-18 | GSE77203 | GEO