Editorial: Cuproptosis and tumors, volume II: from basic research to clinical translation

Copper is an essential trace element involved in mitochondrial metabolism, redox regulation, and enzymatic activity, and its homeostasis is critical for cell survival (Li et al., 2022). Cuproptosis is a newly defined form of regulated cell death (RCD) based on copper ion overload, whose mechanism differs from other RCDs such as apoptosis, necroptosis, pyroptosis, and ferroptosis (Tsvetkov et al., 2022). Copper mediates cuproptosis by directly binding to acyl-transferase enzymes in the tricarboxylic acid cycle, triggering protein aggregation and destabilizing iron-sulfur clusters. Extensive research has demonstrated that cuproptosis is closely linked to tumor metabolism and progression, positioning this pathway as a potential target for cancer mechanism studies and therapeutic interventions (Zhou et al., 2025). CRGs not only serve as a potential biomarker for early diagnosis and prognostic assessment of cancer metastasis, but cuproptosis-based nanomedicines have also been developed for precision synergistic anti-metastatic therapy (Li, Liu, et al., 2025). The core objective of this Research Topic is to deepen our understanding of the mechanisms linking cuproptosis and tumor, thereby paving the way for novel approaches to tumor diagnosis, prognosis assessment, and treatment through the exploitation of cuproptosisrelated mechanisms.