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Targeting the EWSR1-FLI1 oncogene-induced protein kinase PKC-β abolishes ewing sarcoma growth

Didier Surdez1, Magdalena Benetkiewicz, Virginie Perrin

  • 1Institut Curie, INSERM U830, Unité de Génétique et Biologie des Cancers, Institut Curie, Unité de génétique somatique, Paris, France.

Cancer Research
|August 30, 2012
PubMed

Insights

Researchers identified protein kinase C beta (PRKCB) as a druggable target for Ewing sarcoma. This discovery offers a new therapeutic strategy for this aggressive cancer in young adults.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ewing sarcoma is a rare, aggressive cancer primarily affecting young adults.
  • The cancer is driven by a specific fusion oncogene, but effective targeted treatments remain limited.

Purpose of the Study:

  • To identify novel, druggable targets for Ewing sarcoma treatment.
  • To investigate the role of protein kinase C beta (PRKCB) in Ewing sarcoma pathogenesis.

Main Methods:

  • Investigated the regulation of PRKCB by the EWSR1-FLI1 oncogene.
  • Analyzed PRKCB's role in histone modification (H3T6 phosphorylation and H3K4 trimethylation).
  • Assessed the effects of PRKCB inhibition on Ewing sarcoma cells in vitro and in vivo using gene expression profiling.

Main Results:

  • PRKCB is transcriptionally activated by the EWSR1-FLI1 oncogene in Ewing sarcoma.
  • PRKCB regulates H3K4 trimethylation maintenance at gene promoters.
  • PRKCB inhibition induced apoptosis in vitro and suppressed tumor growth in vivo.
  • Gene expression profiling showed significant overlap between EWSR1-FLI1 and PRKCB targets.

Conclusions:

  • PRKCB is a disease-specific, druggable target for Ewing sarcoma.
  • Targeting PRKCB represents a promising preclinical strategy for Ewing sarcoma treatment.

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