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ELK3 promotes cisplatin resistance in ovarian cancer via regulating CHD4 gene expression

Qihua Peng1, Kaho Leung1, Yixuan Sun1

  • 1Shanghai Sixth People's Hospital Affiliated with Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Discover Oncology
|May 19, 2026
PubMed
Abstract

Insights

ELK3 upregulation drives cisplatin resistance in ovarian cancer (OC) by affecting CHD4 and histone lactylation. Targeting the ELK3-CHD4 pathway may overcome chemoresistance in OC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Cisplatin resistance is a significant challenge in ovarian cancer (OC) treatment.
  • The role of ELK3 (ETS transcription factor) in OC chemoresistance is not well understood.

Purpose of the Study:

  • To investigate the role and molecular mechanisms of ELK3 in OC cisplatin resistance.
  • To explore the ELK3-CHD4-histone lactylation axis as a potential therapeutic target.

Main Methods:

  • Analyzed ELK3 expression in OC cells and tissues (qPCR, Western blotting).
  • Performed functional assays (CCK-8, apoptosis, xenografts) to assess ELK3 impact.
  • Investigated mechanisms using Co-IP and histone lactylation analysis.

Main Results:

  • ELK3 was upregulated in resistant OC tissues/cells, correlating with poor survival.
  • ELK3 knockdown sensitized cells to cisplatin by reducing CHD4 and histone lactylation.
  • Restoring CHD4 rescued cisplatin resistance in ELK3-deficient cells.

Conclusions:

  • The ELK3-CHD4-histone lactylation axis is crucial for OC cisplatin resistance.
  • This pathway represents a potential therapeutic target for overcoming chemoresistance in ovarian cancer.
Keywords:
CHD4Cisplatin resistanceELK3Histone lactylationOvarian cancer

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