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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.
Abstract:
It has been a widely held notion within the biomedical research community that the reliable modulation of transcription factors with small molecules would represent a holy grail, given their role in directly potentiating oncogenic programs. Among the transcription factors that have been held in highest regard is Myc, since its dysregulation is among the most recurrent events in human cancer. Despite intense efforts, the ability to identify compounds that bind directly to Myc, resulting in its functional inhibition, have been met with only moderate success. However, a new approach reported by Struntz et al. (Cell Chem. Biol., 2019) focuses on a different strategy of discovering molecules that bind to Myc's obligate partner Max. Using a small-molecule microarray screen, they report the identification of KI-MS2-008, a compound that results in the stabilization of Max homodimers and the attenuation of Myc. KI-MS2-008 suppresses cancer cell grown both in vitro and within in vivo models.
Insights
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.
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.
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