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Life sciences · Journal article
Journal of Nanobiotechnology · October 1, 2026
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Acquired cisplatin resistance remains a major challenge in cancer therapy and is frequently associated with enhanced RAD51-mediated homologous recombination (HR) repair. Here, we identify the CD2 domain of the pluripotency factor NANOG as a previously unrecognized inhibitor of HR repair. Mechanistically, the CD2 peptide interacts with RAD51, thereby impairing nucleofilament assembly and limiting the repair of DNA double-strand breaks. To facilitate intracellular delivery of this macromolecular cargo, we engineered a cell-penetrating peptide (CPP)-functionalized ZIF-8 nanoplatform. This nanosystem promoted cellular uptake, endosomal escape, and subsequent nuclear localization of CD2. Importantly, the truncated CD2 fragment retained HR-inhibitory activity while lacking the transcriptional domains present in full-length NANOG that are associated with stemness-related and oncogenic functions. Functionally, intracellular delivery of CD2 suppressed HR repair activity and enhanced cisplatin sensitivity in both parental and cisplatin-resistant cervical cancer cells. Upon cisplatin treatment, the nanoplatform increased DNA damage and apoptotic responses, leading to greater cytotoxic effects in vitro. Collectively, these findings demonstrate that combining endogenous protein–protein interaction modulation with nanodelivery strategies represents a feasible approach for targeting HR repair and improving cisplatin responsiveness in cervical cancer cells.