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MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Jitendra K Meena1,2, Jarey H Wang2,3, Nicholas J Neill1,2,4
1Therapeutic Innovation Center (THINC), Baylor College of Medicine, Houston, Texas.
Cancer Discovery
|August 28, 2024
Summary
MYC upregulation in cancer triggers excess RNA decay, leading to cell death via toxic byproducts. Inhibiting purine salvage pathways can impair MYC-driven tumor growth, offering new therapeutic strategies.
Area of Science:
- Molecular Biology
- Cancer Biology
- Metabolomics
Background:
- MYC oncogene drives cancer by increasing gene expression and RNA synthesis.
- Consequences of elevated RNA levels and associated metabolic stress in cancer are not well understood.
Purpose of the Study:
- Investigate the role of RNA degradation and ribonucleotide catabolism in MYC-driven cancer.
- Identify novel therapeutic vulnerabilities in MYC-amplified cancers.
Main Methods:
- Utilized genetic manipulation and metabolomic profiling.
- Studied the cytoplasmic exosome pathway in RNA decay.
- Assessed the impact of purine salvage pathways.
Main Results:
- MYC overexpression enhances RNA decay via the cytoplasmic exosome.
- Increased RNA decay leads to accumulation of cytotoxic catabolites and reactive oxygen species.
- Inhibition of purine salvage impairs MYC-driven tumor progression.
Conclusions:
- MYC-induced RNA decay represents a novel oncogenic stress and a potential therapeutic target.
- Targeting purine salvage pathways offers a tractable approach for treating MYC-driven cancers, including Triple-Negative Breast Cancer (TNBC).
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