Erastin

Erastin is a ferroptosis activator by acting on mitochondrial VDAC, exhibiting selectivity for tumor cells bearing oncogenic RAS. (In Vitro) :Erastin (10 μM; 24 h) triggers ferroptosis in ectopic endometrial stromal cells (EESCs), and increases the total ROS level at 9 h.Erastin shorts mitochondria and increases membrane density in EESCs.Erastin (10 μM; 9 h) decreases the mRNA expression levels of iron-related proteins, such FPN (iron exporter) in EESCs. However, FPN overexpression significantly inhibits erastin-induced ferroptosis in EESCs.Erastin (10 μM; 24 h) induces mitochondrial permeability transition pore (mPTP) opening in HT-29 colorectal cancer cells.Erastin (30 μM; 72 h) significantly inhibits the growth of HT-29 colorectal cancer cells.The molecular mechanism by which Erastin induces ferroptosis is related to genes regulating iron or mitochondrial fatty acid metabolism. Includes ribosomal protein L8, iron response element binding protein 2 (IREB2), ATP synthase F0 complex subunit C3, citrate synthase, tetrapeptide repeat domain 35, and acyl-CoA synthetase family member 2 (ACSF2) . (In Vivo) :Erastin (40 mg/kg; i.p.; once every 3 days for 2 weeks) suppresses endometriotic implants in the mouse endometriosis model, indicating Erastin regresses ectopic lesions by trigging ferroptosis.Erastin (10 mg/kg, 30 mg/kg; i.p.; once daily.