GDF15-GFRAL orchestrates glutathione synthesis via NRF2-elicited GCLC activation to impedes cuproptosis
This study identified a non-canonical function of GDF15-GFRAL pathway that plays oncogenic roles and modulates cuproptosis by mediating GSH addiction in SCC. To identify the critical regulatory of cuproptosis, we performed RNA-seq in parental and DTP (EC) cells. Overall design: RNA-seq of parental and drug tolerant persister (DTP) KYSE450 cells