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September 16, 2025eLifeOpen Access

SETD2 suppresses tumorigenesis in a KRASG12C-driven lung cancer model, and its catalytic activity is regulated by histone acetylation

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Authors

RMRicardo J MackTowson UniversityNFNatasha FloresThe University of Texas MD Anderson Cancer CenterGFGeoffrey FoxUniversity of North Carolina at Chapel Hill

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Implication

Research demonstrates SETD2 enhances H3K36 methylation driven by histone acetylation, indicating tumor suppression mechanisms in KRAS G12C lung cancer.

Key Points

  • SETD2 functions as a tumor suppressor, and its activity is enhanced by histone acetylation.
  • Analyzed effects reveal that Setd2 ablation leads to increased cancer lethality in a KRAS G12C-driven model.
  • Biochemical studies indicate that polyacetylation of histones significantly promotes SETD2's methylation activity.
  • Study findings highlight the role of SETD2-associated epigenetic changes in cancer pathogenesis.

Cite This Study

Mack et al. (2025) studied this question.

synapsesocial.com/papers/68d454cb31b076d99fa5a3b4https://doi.org/10.7554/elife.107451.3
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