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Castalin Induces ROS Production, Leading to DNA Damage and Increasing the Activity of CHK1 Inhibitor in Cancer Cell
Margherita D'Angelo1,2, Annamaria Medugno2,3, Maria Cuomo2,3
1Dipartimento di Salute Mentale, Fisica e Medicina Preventiva, Università degli Studi della Campania "Luigi Vanvitelli", 80131 Napoli, Italy.
Antioxidants (Basel, Switzerland)
|September 27, 2025
Summary
Castalin from chestnut shells induces DNA damage and shows potential synergy with CHK1 inhibitors. This natural compound may offer a new cancer therapy approach with reduced side effects.
Area of Science:
- Natural Product Chemistry
- Cancer Biology
- Molecular Oncology
Background:
- Cancer therapy faces challenges due to side effects from chemotherapy and targeted treatments.
- Discovering novel molecules for reduced side effects and new therapeutic strategies is a key research area.
Purpose of the Study:
- To identify and characterize castalin from chestnut shells as a potential anti-cancer agent.
- To evaluate castalin's efficacy alone and in combination with a CHK1 inhibitor for cancer treatment.
Main Methods:
- Castalin isolation and identification using NMR and LC-MS/MS.
- Treatment of cancer cell lines with castalin and a CHK1 inhibitor (SRA737).
- RNA-sequencing analysis of castalin-treated HeLa cells.
Main Results:
- Castalin induces DNA damage, likely via increased reactive oxygen species (ROS) production.
- Antioxidant treatment (ascorbic acid) mitigated castalin-induced DNA damage.
- Castalin demonstrated a synergistic effect with the CHK1 inhibitor SRA737.
Conclusions:
- Castalin induces DNA damage and promotes Non-Homologous End Joining (NHEJ) DNA repair.
- Combining castalin with SRA737 enhances CHK1 inhibitor efficacy and may reduce side effects.
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