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KDM5D expression is lost in cisplatin‑resistant neuroblastoma cells
Natalia Podhorska1, Jan Hrabeta1, Marie Belhajova1
1Department of Pediatric Hematology and Oncology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, 150 06 Prague 5, Czech Republic.
Oncology Reports
|March 6, 2026
Summary
Loss of KDM5D expression in neuroblastoma cells correlates with cisplatin chemoresistance, potentially mediated by increased CUL4A. Restoring KDM5D can reverse this resistance, suggesting KDM5D and CUL4A as therapeutic targets.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Chemoresistance significantly hinders cancer therapy success.
- Histone lysine demethylase dysregulation is implicated in various cancers.
- The KDM5 family may influence oncogene/tumor suppressor balance and drug tolerance.
Purpose of the Study:
- To investigate the role of KDM5D in cisplatin chemoresistance in high-risk neuroblastoma.
- To explore the relationship between KDM5D, CUL4A, and neuroblastoma chemoresistance.
Main Methods:
- Analysis of KDM5D and CUL4A expression in cisplatin-sensitive and resistant neuroblastoma cell lines.
- Gene silencing of KDM5D and ectopic KDM5D expression experiments.
- Assessment of neuroblastoma cell proliferation, migration, cell death, and cell cycle phase.
Main Results:
- KDM5D expression was lost in cisplatin-resistant neuroblastoma cells.
- Resistant cells showed increased CUL4A expression.
- KDM5D silencing promoted aggressive phenotypes and cisplatin resistance via CUL4A.
- Ectopic KDM5D expression reversed these effects.
Conclusions:
- KDM5D downregulation contributes to cisplatin chemoresistance in neuroblastoma.
- CUL4A upregulation is associated with KDM5D loss and chemoresistance.
- KDM5D and CUL4A represent potential biomarkers and therapeutic targets for neuroblastoma chemoresistance.
