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Updated: Jun 6, 2025

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HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond

Martina Minisini1, Martina Mascaro1, Claudio Brancolini1

  • 1Laboratory of Epigenomics, Department of Medicine, Università degli Studi di Udine, Udine 33100, Italy.

Cancer Drug Resistance (Alhambra, Calif.)
|December 3, 2024
PubMed

Insights

Histone deacetylases (HDACs) contribute to cancer drug resistance by altering gene expression through epigenetic modifications. Understanding these HDAC mechanisms is crucial for overcoming treatment challenges and preventing cancer recurrence.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Cancer drug resistance and recurrence pose significant clinical challenges.
  • Epigenetic alterations, particularly changes in histone acetylation, are implicated in treatment failure.
  • Histone deacetylases (HDACs) are key regulators of chromatin structure and gene expression.

Purpose of the Study:

  • To review the role of HDACs in the development of cancer drug resistance.
  • To elucidate the epigenetic mechanisms by which HDACs contribute to treatment failure.
  • To highlight potential therapeutic strategies targeting HDACs to overcome resistance.

Main Methods:

  • Literature review of studies investigating HDACs and cancer drug resistance.
  • Analysis of epigenetic mechanisms involving histone acetylation and HDAC targets.
  • Examination of HDAC's influence on gene expression, including promoters and enhancers.

Main Results:

  • HDACs regulate gene expression by controlling histone acetylation and DNA accessibility.
  • Dysregulation of HDACs can lead to altered expression of genes involved in drug sensitivity.
  • Non-histone targets of HDACs also contribute to the development of drug resistance.

Conclusions:

  • HDACs are critical mediators of epigenetic changes that drive cancer drug resistance.
  • Targeting HDACs offers a promising strategy to re-sensitize tumors to chemotherapy and other cancer treatments.
  • Further research into HDAC functions and non-histone targets is needed to optimize therapeutic interventions.
Keywords:
DNA damageHDACsPARPacetylationchemotherapyhormone deprivationpalbociclib

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