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Isolation of the Side Population in Myc-induced T-cell Acute Lymphoblastic Leukemia in Zebrafish
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Max-imizing the Attenuation of Myc Using Small Molecules.

Shelton R Boyd1, Damian W Young2

  • 1Center for Drug Discovery (CDD), Baylor College of Medicine, Houston, TX 77030, USA; Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, TX 77030, USA.

Trends in Pharmacological Sciences
|July 9, 2019
PubMed
Summary

Researchers identified a novel compound, KI-MS2-008, that targets the Myc-binding protein Max. This small molecule stabilizes Max homodimers, inhibiting Myc activity and suppressing cancer cell growth in vitro and in vivo.

Keywords:
MaxMycsmall-molecule microarraystranscription factors

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Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • Transcription factors like Myc are crucial in oncogenic programs.
  • Dysregulated Myc is a common event in human cancers.
  • Targeting Myc directly with small molecules has proven challenging.

Purpose of the Study:

  • To identify small molecules that inhibit Myc function by targeting its partner, Max.
  • To explore a novel therapeutic strategy for Myc-driven cancers.

Main Methods:

  • Utilized a small-molecule microarray screen to identify compounds binding to Max.
  • Investigated the effect of identified compounds on Max homodimerization and Myc activity.
  • Assessed the efficacy of lead compounds in suppressing cancer cell growth.

Main Results:

  • Identified KI-MS2-008, a compound that binds to Max.
  • KI-MS2-008 stabilizes Max homodimers, leading to attenuation of Myc.
  • KI-MS2-008 demonstrated suppression of cancer cell growth in vitro and in vivo models.

Conclusions:

  • Targeting Myc's partner, Max, is a viable strategy for inhibiting Myc.
  • KI-MS2-008 represents a promising lead compound for developing novel cancer therapeutics.
  • This approach offers a new avenue for modulating transcription factor activity in cancer treatment.