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<p>Ovarian cancer patients with platinum resistance face a dismal five-year survival rate of only 30%, owing to the limited efficacy of current therapeutic options. Existing research often focuses on individual epigenetic modifications, which hampers a systematic understanding of resistance mechanisms and their clinical translation. To address this, our review integrates current evidence to propose an “Epigenetic Resistance Stability Network” model, which comprises three core components: (i) four foundational layers, each with distinct roles in cisplatin resistance. These include DNA methylation (e.g., SFRP5 hypermethylation activating the Wnt pathway), non-coding RNAs (ncRNAs), RNA modifications, and histone modifications, which govern gene expression, post-transcriptional regulation, RNA function, and chromatin architecture, respectively. (ii) three interactive networks: “DNA methylation/miRNA feedback loops,” “lncRNA/histone modification cascades,” and “circRNA/m6A synergistic stabilization.” These networks sustain the resistant phenotype by interlinking key nodes across the four foundational layers. (iii) a theoretical framework encompassing two parts: the “Epigenetic Compensation Network” theory (explaining how tumors evade single-target therapies) and the “Epigenetic Temporal Regulation” model (outlining resistance progression: “miRNA response → methylation consolidation → chromatin stabilization”). Building on this model, we outline a translational roadmap involving “biomarker validation (e.g., <i>SFRP5</i> methylation, circITGB6),” “combination therapy development,” and “personalized intervention,” offering novel insights for overcoming cisplatin resistance and improving patient outcomes in ovarian cancer.</p>

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Targeting epigenetic networks to overcome cisplatin resistance in ovarian cancer: from mechanisms to clinical translation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月27日

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  • Maoyan Tang,
  • Yu Wang,
  • Yaya Xie,
  • Jia Li,
  • Danni Ding,
  • Chan Li,
  • Qiaochu Chen,
  • Fengjuan Han

摘要

Ovarian cancer patients with platinum resistance face a dismal five-year survival rate of only 30%, owing to the limited efficacy of current therapeutic options. Existing research often focuses on individual epigenetic modifications, which hampers a systematic understanding of resistance mechanisms and their clinical translation. To address this, our review integrates current evidence to propose an “Epigenetic Resistance Stability Network” model, which comprises three core components: (i) four foundational layers, each with distinct roles in cisplatin resistance. These include DNA methylation (e.g., SFRP5 hypermethylation activating the Wnt pathway), non-coding RNAs (ncRNAs), RNA modifications, and histone modifications, which govern gene expression, post-transcriptional regulation, RNA function, and chromatin architecture, respectively. (ii) three interactive networks: “DNA methylation/miRNA feedback loops,” “lncRNA/histone modification cascades,” and “circRNA/m6A synergistic stabilization.” These networks sustain the resistant phenotype by interlinking key nodes across the four foundational layers. (iii) a theoretical framework encompassing two parts: the “Epigenetic Compensation Network” theory (explaining how tumors evade single-target therapies) and the “Epigenetic Temporal Regulation” model (outlining resistance progression: “miRNA response → methylation consolidation → chromatin stabilization”). Building on this model, we outline a translational roadmap involving “biomarker validation (e.g., SFRP5 methylation, circITGB6),” “combination therapy development,” and “personalized intervention,” offering novel insights for overcoming cisplatin resistance and improving patient outcomes in ovarian cancer.