TY  - EJOU
AU  - Hu, Zhiqing 
AU  - Ma, Lisha 
AU  - Zhu, Weili 

TI  - Research Progress on Cuproptosis in Cisplatin-Resistant Ovarian Cancer
T2  - BIOCELL

PY  - 
VL  - 
IS  - 
SN  - 1667-5746

AB  - Ovarian cancer (OC) is the most lethal gynecologic malignancy. The current first-line treatment still relies primarily on cisplatin-based chemotherapy, yet cisplatin resistance strongly predicts poor patient prognosis. Cuproptosis is a newly identified cell death modality driven by copper overload and impaired mitochondrial respiration. This review outlines the core molecular mechanisms of cuproptosis and examines its complex association with cisplatin resistance in ovarian cancer. Their interplay involves shared transport systems. In cisplatin-resistant ovarian cancer cells, copper influx transporter Copper Transporter 1 (CTR1) downregulation and efflux transporter ATPase copper transporting alpha/beta polypeptide (ATP7A/B) upregulation reduce the intracellular cisplatin concentration and concurrently disrupts copper homeostasis. Furthermore, metabolic reprogramming in cisplatin-resistant cells—including elevated tricarboxylic acid (TCA) cycle activity as a survival adaptation—provides the metabolic basis for cuproptosis. Targeted induction of cuproptosis in ovarian cancer cells thus represents a promising strategy to reverse cisplatin resistance. Currently, copper ionophores that induce cuproptosis have emerged as a research hotspot for overcoming cisplatin resistance, though this strategy faces substantial challenges. Further insights into cuproptosis mechanisms and advances in nanomaterials will ultimately enable targeted cuproptosis induction in tumor cells. It potentially offers new and effective treatment options for patients who experience chemotherapy failure due to cisplatin resistance.
KW  - Cuproptosis; ovarian cancer; cisplatin resistance; copper transporter 1 (CTR1); ATPase copper transporting alpha/beta polypeptide (ATP7A/B)

DO  - 10.32604/biocell.2026.077860