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Macrophages, platelets, and mesenchymal stem cells contribute to the EMT at primary sites, allowing for tumor cells to separate from neighboring epithelial cell-to-cell contacts and acquire an invasive phenotype

Lancet 362, 11421151

FIN56 is an another classic ferroptosis inducer, where the graphdiyne nanoplatforms GDY-FIN56-RAP effectively promotes FIN56-mediated selective lysosomal degradation of GPX4, exhibiting potential anti-glioma efficacy[121]