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Zebrafish Model of Neuroblastoma Metastasis
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Zebrafish Model of Neuroblastoma Metastasis

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Targeting MYCN: a good BET for improving neuroblastoma therapy?

Robert W Schnepp1, John M Maris

  • 1Division of Oncology and the Center for Childhood Cancer Research. The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA.

Cancer Discovery
|March 12, 2013
PubMed

Insights

Targeting MYC oncoproteins in cancer is challenging. Researchers found that inhibiting bromodomain and extraterminal (BET) proteins effectively reduces MYCN levels in neuroblastoma, offering a new strategy against this difficult cancer target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • The MYC oncoprotein family, including MYCN, is a critical driver in various cancers.
  • Directly targeting MYC proteins has proven difficult in drug development.
  • Neuroblastoma is a pediatric cancer often driven by MYCN amplification.

Purpose of the Study:

  • To investigate the therapeutic potential of targeting the bromodomain and extraterminal (BET) protein family in neuroblastoma.
  • To determine if BET protein inhibition can impact MYCN levels and cellular viability.

Main Methods:

  • Pharmacological inhibition of BET proteins in neuroblastoma cell lines.
  • Assessment of MYCN protein levels following BET inhibition.
  • Evaluation of cellular cytotoxicity and anti-cancer effects.

Main Results:

  • Pharmacological interference with BET proteins led to potent depletion of MYCN in neuroblastoma cells.
  • This depletion resulted in significant cellular cytotoxicity.
  • The findings suggest a novel therapeutic strategy targeting a previously undruggable oncogene.

Conclusions:

  • Bromodomain and extraterminal (BET) protein inhibition is a promising strategy for neuroblastoma treatment.
  • Targeting BET proteins offers a novel approach to address the challenge of MYC-driven cancers.
  • This research opens new avenues for developing therapies against MYC-driven oncogenesis.

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