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. 2022 Nov 25;49(1):16. doi: 10.3892/or.2022.8453

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Copyright: © Zhao et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — Knockdown of GPX4 overcomes the resistance to cisplatin in BC cells. (A) T24/R and 5637/R cells were transfected as indicated, and the GPX4 mRNA levels were assessed. (B) T24/R and 5637/R cells were transfected as indicated, and the protein levels of GPX4 were determined. (C) T24/R and 5637/R cells were transfected as indicated, and the cells were treated with the indicated concentrations of cisplatin for 24 h, and the cellular viabilities were assessed. (D) T24/R and 5637/R cells were treated as indicated, and cellular death was detected. (E) T24/R and 5637/R cells were treated as indicated, and the reactive oxygen species levels were assessed. (F) T24/R and 5637/R cells were treated as indicated, and the iron levels were determined. (G) T24/R and 5637/R cells were treated as indicated, and the glutathione levels were detected. (H) T24/R and 5637/R cells were treated as indicated, and lipid peroxidation levels were assessed. Data are presented as the mean ± standard deviation. *P<0.05 and **P<0.01. GPX4, glutathione peroxidase 4; BC, bladder cancer; sh, short hairpin RNA; NC, negative control; ROS, reactive oxygen species; GSH, glutathione; MDA, malondialdehyde.