Fig. 1: Cell model characterisation. | Cell Death & Differentiation

Fig. 1: Cell model characterisation.

From: Loss of BOK increases vulnerability of p53 deficient non-small cell lung cancer cells to ATR inhibition through its role in uridine metabolism

Fig. 1: Cell model characterisation.

A549 lung cancer cells, originally WT for p53, with or without CRISPR induced BOK and/or p53 deletion. A Western blot analysis demonstrating efficient loss of BOK and p53 expression. B Viability data by flow cytometry (AnnexinV/PI exclusion) of cells treated with 20 µM Nutlin 3a for 48 h (N = 9). Murine cell lines derived from mice, originally on a WT p53 genetic background, with mutant KRAS-MYC driven NSCLC, with or without a CRISPR induced deletion of BOK. Whereas line #1 still expresses WT p53, line #2 has lost functional p53 due to loss-of-function missense mutations C Western blot demonstrating BOK knockout efficacy and induction of p53 in line #1 but not line #2. D Viability data by flow cytometry (AnnexinV/PI exclusion) of cells treated with 20 µM Nutlin 3a for 48 h (N = 9). Statistical analysis was performed by two-way ANOVA, followed by pairwise Bonferroni-adjusted T-tests. *: p ≤ 0.05; **: p ≤ 0.01; ***: p ≤ 0.001; ****: p ≤ 0.0001.

Back to article page