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Despite elevated intracellular GSH levels and increased redox cycling activity, the transcriptomic data indicated downregulation of Gss (glutathione synthetase), Gclc (glutamate cysteine ligase catalytic), and Chac1 (a canonical GSH-degrading enzyme), alongside significant upregulation of Chac2, a less characterized homolog involved in glutathione regulation (Fig

Moreover, studies indicate that PDAC cells, through TGF-1 and lysophosphatidic acid (LPA) signaling, induce mPSCs to adopt a more myCAF-like phenotype, which then secretes type I collagen to suppress tumor dissemination [41, 68, 69]