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Published on: October 28, 2019
Myc inhibition impairs autophagosome formation
Pearl P C Toh1, Shouqing Luo, Fiona M Menzies
1Department of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY, UK.
Human Molecular Genetics
|August 13, 2013
Summary
Targeting Myc in cancer therapy inhibits autophagy by reducing JNK1 and Bcl2 phosphorylation. This finding is crucial for developing effective cancer treatments, especially for therapy resistance.
Area of Science:
- Molecular Biology
- Cancer Research
- Cellular Processes
Background:
- Autophagy is a cellular process involved in clearing long-lived proteins and organelles, and it plays a significant role in cancer development.
- Myc is a proto-oncogene frequently deregulated in various cancers, making it a key target for anti-cancer therapies.
Purpose of the Study:
- To investigate the relationship between anti-Myc strategies and autophagy.
- To understand how targeting Myc impacts autophagy and its substrates.
- To explore the molecular mechanisms linking Myc suppression to autophagy inhibition.
Main Methods:
- Depletion of Myc in cancer cells.
- Assessment of autophagosome formation and autophagy substrate clearance.
- Analysis of c-Jun N-terminal kinase 1 (JNK1) and B-cell lymphoma 2 (Bcl2) phosphorylation.
- Measurement of reactive oxygen species (ROS) production.
Main Results:
- Myc depletion was found to inhibit autophagosome formation and impair the clearance of autophagy substrates.
- Suppression of Myc led to reduced phosphorylation of JNK1 and Bcl2, indicating an inhibitory effect on autophagy.
- Decreased JNK1 phosphorylation due to Myc knockdown was correlated with reduced ROS production.
Conclusions:
- Myc suppression inhibits autophagy through the downregulation of JNK1 and Bcl2 phosphorylation.
- Targeting Myc in cancer therapy may offer an additional benefit by inhibiting autophagy, particularly in cases of chemotherapy-induced autophagy resistance.
- These findings highlight the potential of Myc-targeted therapies in overcoming treatment resistance associated with autophagy.
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