Max-imizing the Attenuation of Myc Using Small Molecules.

Autor: Boyd SR; Center 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., Young DW; Center 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; Therapeutic Innovations Center (THINC@BCM), Baylor College of Medicine, Houston, TX 77030, USA; Department of Pathology and Immunology, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: damiany@bcm.edu.
Jazyk: angličtina
Zdroj: Trends in pharmacological sciences [Trends Pharmacol Sci] 2019 Sep; Vol. 40 (9), pp. 608-612. Date of Electronic Publication: 2019 Jul 04.
DOI: 10.1016/j.tips.2019.06.002
Abstrakt: 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.
(Copyright © 2019. Published by Elsevier Ltd.)
Databáze: MEDLINE
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