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Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
09:58

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis

Published on: June 27, 2020

EWS and RE1-Silencing Transcription Factor Inhibit Neuronal Phenotype Development and Oncogenic Transformation in

Savita Sankar1, Nicholas C Gomez, Russell Bell

  • 1Department of Oncological Sciences, University of Utah School of Medicine, Salt Lake City, UT, USA.

Genes & Cancer
|September 27, 2013
PubMed

Insights

Wild-type EWSR1 (EWS) and the EWS/FLI oncoprotein co-regulate genes in Ewing sarcoma. EWS interacts with REST to suppress neuronal development and oncogenic transformation, offering potential therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • EWSR1 gene translocations create oncoproteins driving cancers like Ewing sarcoma.
  • The oncogenic EWS/FLI fusion protein is key in Ewing sarcoma, but wild-type EWS function is unclear.

Purpose of the Study:

  • Investigate the role of wild-type EWSR1 (EWS) in Ewing sarcoma pathogenesis.
  • Identify EWS-regulated genes and cellular processes.
  • Explore the interplay between EWS and EWS/FLI.

Main Methods:

  • RNA interference and RNA sequencing to identify EWS-regulated genes.
  • Functional annotation and co-immunoprecipitation analyses.
  • Genome-wide chromatin binding analysis.

Main Results:

  • EWS and EWS/FLI co-regulate a subset of genes.
  • EWS interacts with REST (RE1-silencing transcription factor) and binds chromatin near NRSE.
  • Both EWS and REST inhibit neuronal phenotype and oncogenic transformation in Ewing sarcoma cells.

Conclusions:

  • Wild-type EWS plays a significant role in Ewing sarcoma phenotype development.
  • EWS and REST cooperate in gene regulation.
  • Modulating EWS function may offer a therapeutic strategy for Ewing sarcoma and related cancers.
Keywords:
EWSEwing sarcomaRESTneuronal phenotypeoncogenic transformation

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