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Targeting the MYC Oncogene in Burkitt Lymphoma through HSP90 Inhibition

Candace J Poole1, Wenli Zheng2, Haesung Lee3

  • 1Department of Biochemistry and Molecular Biology, Augusta University, 1410 Laney-Walker Blvd., Augusta, GA 30912, USA. capoole@augusta.edu.

Cancers
|November 21, 2018
PubMed

Insights

Targeting the MYC oncogene in Burkitt lymphoma is challenging. This study shows HSP90 inhibitors reduce MYC expression by suppressing transcription and destabilizing the protein, offering a new therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Overexpression of the MYC oncogene is common in Burkitt lymphoma.
  • MYC is a difficult therapeutic target, and effective inhibitors are lacking.

Purpose of the Study:

  • To investigate targeting MYC indirectly by inhibiting heat shock protein 90 (HSP90).
  • To evaluate HSP90 inhibitors as a potential therapeutic strategy for Burkitt lymphoma.

Main Methods:

  • Treatment of Burkitt lymphoma cell lines with HSP90 inhibitors (17-AAG, 17-DMAG).
  • Assessing MYC expression, transcription, and protein stability.
  • Combination treatment with HSP90 and proteasome inhibitors.
  • Co-immunoprecipitation assays to determine MYC-HSP90 interaction.

Main Results:

  • HSP90 inhibition reduced MYC expression via suppressed transcription and protein destabilization.
  • HSP90 inhibitors decreased proliferation of Burkitt lymphoma cells.
  • MYC was identified as an HSP90 client protein, degraded by the proteasome upon HSP90 inhibition.

Conclusions:

  • HSP90 inhibitors represent a viable alternative strategy for targeting the MYC oncogene in Burkitt lymphoma.
  • Inhibiting HSP90 effectively reduces MYC levels and tumor cell proliferation.
Keywords:
17-AAG17-DMAGBurkitt lymphomaHSP90MYC

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