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Updated: Mar 22, 2026

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
Published on: May 21, 2019
Strategically targeting MYC in cancer
Valeriya Posternak1, Michael D Cole2
1Department of Pharmacology and Toxicology, Geisel School of Medicine at Dartmouth, Norris Cotton Cancer Center, Lebanon, NH, USA.
Abstract:
MYC is a major driver of cancer cell growth and mediates a transcriptional program spanning cell growth, the cell cycle, metabolism, and cell survival. Many efforts have been made to deliberately target MYC for cancer therapy. A variety of compounds have been generated to inhibit MYC function or stability, either directly or indirectly. The most direct inhibitors target the interaction between MYC and MAX, which is required for DNA binding. Unfortunately, these compounds do not have the desired pharmacokinetics and pharmacodynamics for in vivo application. Recent studies report the indirect inhibition of MYC through the development of two compounds, JQ1 and THZ1, which target factors involved in unique stages of transcription. These compounds appear to have significant therapeutic value for cancers with high levels of MYC, although some effects are MYC-independent. These approaches serve as a foundation for developing novel compounds to pharmacologically target MYC-driven cancers.
Insights
Targeting MYC (Myc) oncoprotein is crucial for cancer therapy. Researchers are developing novel compounds that indirectly inhibit MYC transcription, showing promise for treating MYC-driven cancers.
Area of Science:
- Oncology
- Molecular Biology
- Drug Discovery
Background:
- The MYC oncoprotein drives cancer progression by regulating genes involved in cell growth, proliferation, metabolism, and survival.
- Targeting MYC is a key strategy in cancer therapy, with various compounds developed to inhibit its function or stability.
- Direct MYC inhibitors targeting the MYC-MAX interaction have shown limitations in pharmacokinetic and pharmacodynamic properties for in vivo use.
Purpose of the Study:
- To review the development of compounds that indirectly inhibit MYC.
- To highlight the therapeutic potential of novel MYC-targeting agents in MYC-driven cancers.
Main Methods:
- Review of recent studies on compounds inhibiting MYC transcription.
- Analysis of indirect inhibition strategies targeting transcription factors.
Main Results:
- Two compounds, JQ1 and THZ1, indirectly inhibit MYC by targeting unique transcription stages.
- These compounds demonstrate therapeutic value in MYC-driven cancers, though some effects may be MYC-independent.
- Current indirect inhibition approaches provide a basis for developing new anti-cancer drugs.
Conclusions:
- Indirect inhibition of MYC through transcription targeting represents a promising therapeutic strategy.
- Novel compounds targeting MYC transcription hold potential for treating various cancers.
- Further research into MYC-targeting agents is essential for advancing cancer therapy.
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