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CoREST Complex Stabilizes MYC Protein to Promote Cancer Cell Genome Stability.
Biorxiv : the Preprint Server for Biology
|January 7, 2025
Summary
The CoREST complex stabilizes MYC protein, regulating RNA splicing. Disrupting this interaction in melanoma alters splicing, impacting cell survival and offering a potential cancer therapy target.
Area of Science:
- Molecular Biology
- Cancer Biology
- RNA Processing
Background:
- RNA maturation involves RNA-binding proteins and pre-mRNA processing.
- MYC influences splicing machinery genes; splicing defects are linked to cancer.
- The CoREST complex's role in cancer is not fully understood.
Purpose of the Study:
- To investigate the CoREST complex's role in MYC stability and RNA processing.
- To determine the impact of CoREST complex disruption on MYC-driven cancers, specifically melanoma.
Main Methods:
- Investigated CoREST complex interaction with MYC.
- Utilized genetic ablation and pharmacological inhibition of the CoREST complex in melanoma cells.
- Analyzed changes in spliceosome activity, genome-wide splicing patterns, and cell viability.
Main Results:
- The CoREST complex stabilizes MYC via deacetylation, acting as a transcriptional coregulator for RNA processing genes.
- Inhibition of the CoREST complex in melanoma alters spliceosome activity and genome-wide alternative splicing.
- Disruption compromises cell survival, partially rescued by NOLC1 expression.
Conclusions:
- The CoREST-MYC interaction is a key regulator of cancer-specific mRNA splicing variants.
- Targeting the CoREST-MYC axis may offer a therapeutic strategy for MYC-driven cancers like melanoma.
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