Fig. 1: SAL suppresses the NF-κB/MUC1-C auto-inductive circuit.
From: MUC1-C is a target of salinomycin in inducing ferroptosis of cancer stem cells
DU-145 (A) and H660 (B) cells were treated with vehicle (DMSO) or the indicated concentrations of SAL for 72 h. Viability was assessed by Alamar Blue staining. The results (mean ± SD of 4 determinations) are expressed as relative viability compared to untreated cells (assigned a value of 100%). C, D DU-145 and H660 cells treated with vehicle or 1 μM SAL for 24 h were analyzed for MUC1-C transcripts using primers listed in Supplementary Table S1 (C). The results (mean ± SD of 4 determinations) are expressed as relative MUC1-C mRNA levels compared to that obtained in vehicle-treated cells (assigned a value of 1). Lysates were immunoblotted with antibodies against the indicated proteins (D). DU-145 (E) and H660 (F) cells expressing a control CshRNA or NF-κBshRNA were analyzed for MUC1-C transcripts (left). The results (mean ± SD of 4 determinations) are expressed as relative MUC1-C mRNA levels compared to that obtained in CshRNA cells (assigned a value of 1). Lysates were immunoblotted with antibodies against the indicated proteins (right). DU-145 (G) and H660 (H) cells left untreated or treated with 10 μM BAY11-7082 for 24 h were analyzed for MUC1-C transcripts (left). The results (mean ± SD of 4 determinations) are expressed as relative MUC1-C mRNA levels compared to that obtained in untreated cells (assigned a value of 1). Lysates were immunoblotted with antibodies against the indicated proteins (right).
