Skip to main content
. 2022 Feb 2;8(5):eabl8920. doi: 10.1126/sciadv.abl8920

Fig. 3. An unbiased bulk RNA-seq of parental HT1080 and GR-crKO cells reveals dexamethasone-induced genes involved in ferroptosis.

Fig. 3.

(A) Protein expression of key players in ferroptosis 12 hours after treatment with or without 1 μM dexamethasone with subsequent treatment of induction of ferroptosis for 18 hours with erastin. β-Actin serves as a loading control. (B) Protein expression of HMOX1, GCLC, and GCLM 12 hours after treatment with or without 1 μM dexamethasone with subsequent treatment of induction of ferroptosis for 18 hours with erastin. β-Actin serves as a loading control. (C) GSH content in HT1080 cells treated with or without 1 μm dexamethasone before inducing ferroptosis with 5 μM erastin for 14 hours. (D) Volcano plot of differently regulated genes upon dexamethasone treatment in HT1080 cells. The bar graph shows means ± SD. Statistical analysis was performed using Student’s t test. *P ≤ 0.05, ****P ≤ 0.0001 (GR: glucocorticoid receptor, ACSL4: acyl-CoA synthetase long chain family member 4, SCL7A11: solute carrier family 7 member 11, GPX4: GSH peroxidase 4, TXNRD1: thioredoxin reductase 1, PRX1: peroxiredoxin 1, TRX: thioredoxin, CBS: cystathionine beta-synthase, CSE: cystathionine gamma lyase, HMOX1: heme oxygenase 1, GCLC: glutamate-cysteine ligase catalytic subunit, GCLM: glutamate-cysteine ligase modifier subunit, GSH: glutathione, n.d.: not detectable).