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PDGF-C is an EWS/FLI induced transforming growth factor in Ewing family tumors

J P Zwerner1, W A May

  • 1Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL, USA.

Oncogene
|April 21, 2001
PubMed

Insights

Aberrant transcription factors drive human cancers. This study identifies Platelet-Derived Growth Factor C (PDGF-C) as a key target of EWS/FLI-1 fusion proteins in Ewing Family Tumors (EFT), suggesting its role in oncogenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Aberrant transcription factors are implicated in human malignancies by deregulating tumorigenic pathways.
  • Ewing Family Tumors (EFT) characteristically involve EWS/ETS fusion proteins, particularly EWS/FLI-1.
  • Identifying downstream targets of these fusion proteins has been challenging.

Purpose of the Study:

  • To identify novel targets of EWS/FLI-1 transcriptional deregulation in EFT.
  • To investigate the role of identified targets in EFT oncogenesis.

Main Methods:

  • Utilized efficient retroviral systems to screen cDNA from EWS/FLI-1 transformed cells.
  • Assessed gene expression and biological activity of potential targets in vitro and in vivo.
  • Investigated the dependency of target gene expression on EWS/FLI-1 activity.

Main Results:

  • Identified Platelet-Derived Growth Factor C (PDGF-C) as a direct transcriptional target of EWS/FLI-1.
  • PDGF-C is expressed in EFT cell lines and primary tumors.
  • PDGF-C expression in EFT cell lines is dependent on EWS/FLI-1 activity.
  • PDGF-C exhibits significant in vitro and in vivo biologic activity.

Conclusions:

  • PDGF-C is a novel, transcriptionally deregulated target of EWS/FLI-1 in EFT.
  • PDGF-C may function as a significant mediator of EWS/FLI-1 driven oncogenesis in Ewing Family Tumors.

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