Uncovering metabolic reprogramming in ovarian and cervical cancers with multi-omics

assays to explore their metabolic reprogramming and therapeutic targets. The results revealed that OC exhibits intratumoral metabolic heterogeneity and suppresses tryptophan and vitamin B6 metabolism, with ferroptosis-related proteins upregulated in metastatic lesions and ALDH7A1/GATM knockdown promoting its cell proliferation and migration. CC progression was marked by amino acid and bile acid accumulation and neomenthol-driven cell proliferation. Purine metabolism activation was identified as a shared hallmark of both cancers, and purine nucleoside phosphorylase (PNP) knockdown was found to inhibit the proliferation of both OC and CC cells. This work identifies stage-specific metabolic vulnerabilities and PNP as a conserved therapeutic target, providing a framework for developing tailored gynecological cancer therapies.