Fig. 5: SLC25A10 promotes DDP resistance in cervical cancer cells by inhibiting ferroptosis.

Cell viability was assessed via light microscopic analysis (A–H). After 24 h of treatment with different concentrations of DDP, less cell death of CaSki and HeLa cells overexpressing SLC25A10 was observed, whereas more cell death was observed in the knockdown group (A, B). HeLa cells in which SLC25A10 was overexpressed or knocked down were treated with 1 µM RSL3, 10 µM erastin or 4 µg/mL DDP for 24 h, and DMSO or NS was used as a control. We found that apoptosis (Z-V) and necrosis (Nec) inhibitors could not prevent RSL3- and erastin-induced cell death. However, a ferroptosis inhibitor (Ferr-1) partially attenuated ferroptosis inducer-induced cell death (C, D, F, G). After the ferroptosis inducer was substituted with DDP, cell death was also reversed by the ferroptosis inhibitor, independent of the use of the apoptosis and necrosis inhibitors (E, H). Scale =10 µm.