HNK synergistically enhances CPT-induced apoptosis in TMZ-resistant glioblastoma cells through CDK1-mediated G2/M arrest and ROS-dependent mitochondrial activation of caspases-9, -3, and -6. Co-administration of HNK may enable effective CPT-based therapy at reduced doses, potentially minimizing CPT-related toxicity and offering a promising strategy for treating drug-resistant GBM.
Yang et al. (Fri,) studied this question.