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Expression profiling of EWS/FLI identifies NKX2.2 as a critical target gene in Ewing's sarcoma

Richard Smith1, Leah A Owen, Deborah J Trem

  • 1The Center for Children, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA.

Cancer Cell
|May 16, 2006
PubMed

Insights

Ongoing EWS/FLI expression drives Ewing sarcoma tumorigenesis. Researchers identified NKX2.2 as a critical EWS/FLI-regulated gene essential for this cancer

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ewing sarcoma development is driven by the EWS/FLI fusion protein.
  • The specific cell of origin for Ewing sarcoma remains poorly understood.
  • Understanding EWS/FLI function within the tumor is crucial.

Purpose of the Study:

  • To investigate the role of EWS/FLI in established Ewing sarcoma.
  • To identify genes regulated by EWS/FLI in Ewing sarcoma.
  • To determine critical EWS/FLI targets involved in oncogenic transformation.

Main Methods:

  • Utilized retroviral-mediated RNA interference to suppress EWS/FLI.
  • Performed reexpression studies to confirm EWS/FLI requirement.
  • Analyzed gene expression profiles to identify EWS/FLI-regulated genes.

Main Results:

  • Confirmed that sustained EWS/FLI expression is necessary for the tumorigenic phenotype.
  • Developed a comprehensive transcriptional profile of EWS/FLI activity.
  • Identified NKX2.2 as a key EWS/FLI-regulated gene essential for transformation.

Conclusions:

  • Ongoing EWS/FLI expression is indispensable for Ewing sarcoma maintenance.
  • NKX2.2 is a critical downstream target of EWS/FLI in Ewing sarcoma.
  • This study provides a validated transcriptional map and identifies a key oncogenic driver.

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