Related Experiment Video

Updated: Jul 10, 2026

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues
10:41

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues

Published on: April 5, 2018

Mechanistic analysis on epigenetic programming of tumor drug resistance

Xiao-Xiao Han1, Kun Pang2, Jia-Hao Sun3

  • 1Department of Urology, The Fourth Affiliated Hospital of Soochow University, Soochow, China.

Drug Resistance Updates : Reviews and Commentaries in Antimicrobial and Anticancer Chemotherapy
|July 8, 2026
PubMed

Insights

Epigenetic mechanisms drive cancer drug resistance by altering gene expression. Targeting these reversible modifications offers a promising strategy to overcome treatment failure and improve patient outcomes.

Area of Science:

  • Oncology
  • Epigenetics
  • Cancer Biology

Background:

  • Drug resistance is a major obstacle in cancer therapy, limiting treatment efficacy and worsening patient prognosis.
  • Drug-tolerant persister (DTP) cells and tumor heterogeneity contribute significantly to therapeutic failure.
  • Understanding the mechanisms of drug resistance is crucial for developing effective cancer treatments.

Purpose of the Study:

  • To review the core epigenetic regulatory mechanisms underlying cancer drug resistance.
  • To elucidate the mechanistic links between epigenetic programming and the acquisition of drug resistance.
  • To highlight the potential of targeting epigenetic modifications for overcoming therapeutic resistance.

Main Methods:

  • Literature review of epigenetic mechanisms in cancer drug resistance.
  • Analysis of DNA methylation, histone modifications, non-coding RNAs (ncRNAs), and N6-methyladenosine (m6A) RNA methylation.
  • Exploration of the metabolism-epigenetic crosstalk axis in drug resistance.

Main Results:

  • Dynamic epigenetic alterations reprogram transcriptional landscapes, enabling cancer cells to evade drug-induced death.
  • Epigenetic modifications, unlike genomic mutations, are pharmacologically reversible.
  • Combinatorial therapies involving epigenetic modulators and conventional agents show promise in reversing resistance.

Conclusions:

  • Epigenetic reprogramming is a key driver of cancer drug resistance.
  • The reversibility of epigenetic changes offers therapeutic opportunities.
  • Targeting epigenetic networks can lead to novel biomarkers and personalized combination therapies for drug-resistant cancers.
Keywords:
BiomarkersDrug resistanceEpigeneticsTherapeutic targets

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