[From driver gene mutations to cell death crosstalk: Ferroptosis regulatory networks and prospects for targeted cancer therapy].
Year: 2026
Type: review
Abstract: mutation subtype, the target used to induce ferroptosis, and treatment status with EGFR tyrosine kinase inhibitors (EGFR-TKIs). Ferroptosis can also crosstalk with apoptosis, necroptosis, pyroptosis, cuproptosis, and disulfidptosis through oxidative stress, iron metabolism, autophagy, mitochondrial function, inflammatory signaling, and nutrient metabolism. Within the tumor microenvironment, immune cells, cancer-associated fibroblasts, and vascular endothelial cells can alter the ferroptosis threshold of tumor cells through cytokines, metabolic substrate supply, and extracellular vesicle-mediated intercellular regulation. Targeting these shared regulatory nodes, or combining ferroptosis induction with targeted therapy, chemotherapy, or immunotherapy, shows clinical potential for overcoming therapeutic resistance. However, translation remains constrained by toxicity to normal tissues, insufficient prognostic and pharmacodynamic biomarkers, suboptimal druggability of candidate agents, and limited delivery efficiency. Therefore, ferroptosis-targeted therapeutic strategies should integrate driver genotype, treatment status, cell type, and the metabolic microenvironment for patient stratification while improving tumor selectivity and treatment monitorability.
Source: PubMed Central
Authors: Yuxiao Li, Yongguang Tao
Institution: Central South University
Language: Chinese
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W7223856004