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January 18, 2026Nucleic Acids ResearchOpen Access

E2F1 K117 methylation by SETD6 disrupts BRD4–E2F1 binding and modulates E2F1 chromatin binding and gene regulation in prostate cancer cells

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Authors

GUGizem T. UluMKMargarita KublanovskyRSRaz Shalev

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Overview

Investigations reveal how SETD6 modifies E2F1, influencing gene regulation and cancer traits in prostate cancer cells, suggesting a broader regulatory mechanism.

Key Points

  • This research aims to explore the role of SETD6-mediated K117 methylation of E2F1 in prostate cancer cells.
  • Conducted chromatin binding and gene expression experiments in prostate cancer cells
  • Utilized biochemical and genomic assays to analyze E2F1 interactions
  • Investigated the effects of E2F1 methylation on oncogenic phenotypes
  • Identified distinct gene sets bound and upregulated by methylated and unmethylated E2F1
  • Demonstrated that K117 methylation prevents K117 acetylation, affecting E2F1 and BRD4 interaction
  • Suggested that K117 methylation acts as a switch regulating E2F1's cellular effects

Cite This Study

Ulu et al. (2026) studied this question.

synapsesocial.com/papers/696c79cde45ebfc9113cd474https://doi.org/10.1093/nar/gkaf1513
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1SETD6 mediates selective interaction and genomic occupancy of BRD4 and MITF in melanoma cells2025
  2. 2Targeting the Tumor Epigenetic Regulator SETDB1 for Tumor Therapy2024 · 3 citations
  3. 3SETD2 suppresses tumorigenesis in a KRASG12C-driven lung cancer model and its catalytic activity is regulated by histone acetylation2025
  4. 4RAD18 methylation by the methyltransferase SETD6 attenuates DNA breaks2025
  5. 5SETD2 suppresses tumorigenesis in a KRASG12C-driven lung cancer model, and its catalytic activity is regulated by histone acetylation2025 · 3 citations