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Updated: Jun 10, 2026
09:44
High-throughput Screening for Chemical Modulators of Post-transcriptionally Regulated Genes
Published on: March 3, 2015
Small-molecule modulators of c-Myc/Max and Max/Max interactions.
1Institute of Organic Chemistry, University of Leipzig, Johannisallee 29, Leipzig, Germany. tberg@uni-leipzig.de
Current Topics in Microbiology and Immunology
|August 4, 2010
Summary
Small molecules targeting the transcription factor c-Myc offer a promising cancer therapy. These compounds inhibit c-Myc by disrupting its interaction with Max or stabilizing Max homodimers, counteracting tumor growth.
Area of Science:
- Oncology
- Molecular Biology
- Drug Discovery
Background:
- The transcription factor c-Myc is frequently overexpressed in human tumors.
- c-Myc's oncogenic functions rely on heterodimerization with its partner, Max.
- Targeting c-Myc protein-protein interactions presents a viable strategy for cancer treatment.
Purpose of the Study:
- To review small organic molecules that inhibit c-Myc.
- To summarize approaches modulating c-Myc/Max protein-protein interactions.
- To highlight therapeutic strategies against c-Myc in cancer.
Main Methods:
- Literature review of small molecules targeting c-Myc.
- Analysis of compounds inhibiting c-Myc/Max heterodimerization.
- Summary of strategies stabilizing Max homodimers.
Main Results:
- Small molecules can effectively inhibit c-Myc/Max interactions.
- Stabilization of Max homodimers reduces c-Myc activity.
- Diverse small organic molecules show potential in modulating these interactions.
Conclusions:
- Targeting c-Myc protein-protein interactions is a key strategy in cancer therapy.
- Small molecules offer a feasible approach to inhibit oncogenic c-Myc.
- Modulating c-Myc/Max interactions holds promise for developing novel cancer treatments.
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