It is demonstrated that combining cuproptosis induction with CSC stemness suppression represents a promising strategy for overcoming chemoresistance, highlighting HS-Cu@DOX as a potential therapeutic candidate for recurrent ovarian cancer.
Abstract
Ovarian cancer remains difficult to treat due to the persistence of chemoresistant cancer stem-like cells (CSCs), which are major drivers of tumor relapse. Herein, we engineered a hyaluronic acid-functionalized nanoplatform (HS-Cu@DOX) via the assembly of a shikonin–copper (SKN-Cu) coordination complex with hyaluronic acid, followed by electrostatic loading of doxorubicin (DOX), enabling tumor-targeted co-delivery of both therapeutic agents. This nanoplatform disrupts intracellular redox homeostasis to induce cuproptosis while concurrently suppressing CSC stemness through downregulation of key pluripotency-associated transcription factors (e.g., SOX2, OCT4, and NANOG). By depleting intracellular glutathione (GSH) and impairing antioxidant defenses, HS-Cu@DOX disrupts the oxidative stress resilience of CSCs, thereby restoring their sensitivity to DOX-induced apoptosis. Consequently, this strategy enhances DOX-mediated cytotoxicity and reduces systemic toxicity while maintaining potent antitumor efficacy. Collectively, our findings demonstrate that combining cuproptosis induction with CSC stemness suppression represents a promising strategy for overcoming chemoresistance, highlighting HS-Cu@DOX as a potential therapeutic candidate for recurrent ovarian cancer.
Tumor chemoresistance, driven by mechanisms such as drug efflux, DNA repair, apoptosis inactivation, immunosuppressive microenvironments, and the maintenance of cancer stem cell (CSC) stemness, remains a major obstacle to effective chemotherapy and patient prognosis. Engineered nanoplatforms offer multifaceted strate...
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Cuproptosis, a novel modality of mitochondrial copper-induced cell death, holds great therapeutic potential against cancer. However, its efficacy is limited by cancer-associated fibroblasts (CAFs), which confer the cuproptosis resistance in tumor by upregulating the copper exporter ATP7A. In this study, we developed an...
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