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. 2020 Dec 14;13(2):e10852. doi: 10.15252/emmm.201910852

Figure EV5. APR‐246 sensitivity is dictated by the presence of mutant p53, cellular thiol status, and drug accumulation.

Figure EV5

  1. Growth suppression of isogenic H1299, Saos‐2 and HCT116 cells with different TP53 status after 72 h APR‐246 treatment, as assessed by the WST‐1 assay (n ≥ 3). The data is also shown in Fig 1A and Appendix Fig S1A, n in Appendix Table S1.
  2. Correlation of PRIMA‐1 AUC with GSH and GSSG abundance in 708 cell lines from the DepMap portal. R and P values were determined by Pearson’s correlation.
  3. Total GSH + GSSG by a GR re‐cycling assay in HCT116 WT and R248W cells 48 h after siRNA p53 transfection. Values are averages of 1‐2 different siRNAs against TP53 and 1‐2 different controls (WT n = 3 R248W n = 2), individual values are shown in Appendix Fig S7K.
  4. 14C‐accumulation (cpm/(mg/ml)) in HCT116 WT and R248W cells 24 h after treatment with 14C‐APR‐246 and 48 h after transfection of siRNAs against p53. Values are averages of 2 different siRNAs against p53 and 2 different controls (WT n = 3 R248W n = 2). Values of individual siRNAs are shown in Appendix Table S4.
  5. Growth suppression in HCT116 WT and R248W cells after 48 h of APR‐246 treatment and 96 h post‐transfection of +/− siRNAs targeting p53 as determined by the WST‐1 assay. Values are averages of 2 different siRNAs against TP53 and 2 different controls (WT n = 5–6 and R248W n = 3) *P = 0.047, Paired t‐test.

Data information: TP53 status is indicated for each cell line. Data are represented as mean ± SEM.