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| Format: | Recurso digital |
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Zenodo
2025
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| Online Access: | https://doi.org/10.5281/zenodo.14715053 |
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Table of Contents:
- <p>Cancer-associated mutation of EZH2 can drive or restrict transformation. We describe here induction of senescence by pharmacologic inhibition of CDK4/6 as the likely major mechanism of action underlying -ciclib function in human cancer, which was intrinsically associated with repression of the proliferation-associated gene EZH2. In human cells, EZH2 repression was an essential component of the senescence gene expression signature. Mechanistically, we discovered stage selective control of CDKN isoform expression by EZH2 in the erythroid lineage, specifically p16ink4A/p14ARF (CDKN2A) and p18ink4C (CDKN2C). EZH2 executes control of both proliferative and senescent cellular programs through stage-specific regulation of CDKN gene expression. </p>