Related Experiment Video

Updated: Oct 29, 2025

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

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Proteasome inhibitors suppress MYB oncogenic activity in a p300-dependent manner

Maria V Yusenko1, Abhiruchi Biyanee1, Mattias K Andersson2

  • 1Institute for Biochemistry, Westfälische-Wilhelms-Universität, Münster, Germany.

Cancer Letters
|July 13, 2021
PubMed

Insights

Proteasome inhibitors, like oprozomib, show potential for targeting MYB in cancers such as acute myeloid leukemia (AML) and adenoid cystic carcinoma (ACC). This study reveals a novel mechanism for suppressing oncogenic MYB activity.

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • MYB is a key driver in human malignancies like acute myeloid leukemia (AML) and adenoid cystic carcinoma (ACC).
  • Targeting transcription factors like MYB presents a therapeutic opportunity, despite challenges in drug development.

Purpose of the Study:

  • To screen FDA-approved drugs for novel MYB inhibitors using a MYB reporter cell line.
  • To investigate the anti-cancer effects of proteasome inhibitors on MYB-driven cancers.

Main Methods:

  • Screening of an FDA-approved drug library against a MYB reporter cell line.
  • Detailed characterization of the proteasome inhibitor oprozomib.
  • Assessing the impact of oprozomib on MYB activity and cancer cell proliferation.

Main Results:

  • Proteasome inhibitors demonstrated significant MYB-inhibitory activity.
  • Oprozomib interfered with the p300 co-activator's stimulation of MYB.
  • Oprozomib exhibited anti-proliferative effects on human AML and ACC cells.

Conclusions:

  • Proteasome inhibition effectively suppresses oncogenic MYB activity.
  • Oprozomib represents a potential therapeutic agent for MYB-driven malignancies.
  • This study identifies a novel therapeutic strategy for AML and ACC.
Keywords:
Adenoid cystic carcinomaInhibitorMYBMyeloid leukemiaProteasome inhibitor

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