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A TFIID-SAGA Perturbation that Targets MYB and Suppresses Acute Myeloid Leukemia

Yali Xu1, Joseph P Milazzo2, Tim D D Somerville2

  • 1Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA; Molecular and Cellular Biology Program, Stony Brook University, New York, NY 11794, USA.

Cancer Cell
|January 10, 2018
PubMed

Insights

Researchers found TAF12 is crucial for acute myeloid leukemia (AML) progression by interacting with the MYB transcription factor. Targeting this interaction offers a new strategy for AML treatment.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Gene Regulation

Background:

  • Targeting general coactivators is a strategy to inhibit oncogenic transcription factors (TFs).
  • Coactivator perturbations can cause broad effects impacting multiple TFs.
  • Acute myeloid leukemia (AML) is driven by aberrant TF activity.

Purpose of the Study:

  • Identify specific coactivator requirements in AML.
  • Investigate the role of TAF12 in leukemogenesis.
  • Develop a targeted approach for AML therapy.

Main Methods:

  • Identified TAF12 as essential for AML progression.
  • Characterized the interaction between TAF12/TAF4 and MYB.
  • Utilized TAF4 histone-fold fragment to inhibit TAF12 function.
  • Tested efficacy in mouse models of AML.

Main Results:

  • TAF12, a subunit of TFIID and SAGA, is selectively required for AML.
  • A direct interaction exists between the TAF12/TAF4 heterodimer and MYB's transactivation domain.
  • Ectopic expression of TAF4 fragment suppressed MYB and led to AML regression in mice.

Conclusions:

  • TAF12 is a key coactivator for the oncogenic TF MYB in AML.
  • Targeting the TAF12-MYB interaction provides a selective strategy for AML treatment.
  • This approach offers a way to neutralize oncogenic TFs by targeting general coactivator complexes.
Keywords:
MYBSAGATAF12TFIIDacute myeloid leukemiacoactivatorepigenetics

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