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. 2021 May 31;118(23):e2019740118. doi: 10.1073/pnas.2019740118

Fig. 3.

Fig. 3.

Genetic priming of lung adenocarcinoma cell lines is sufficient to switch cell fate of p53-restored cells from cell cycle arrest to apoptosis. (A) CRISPR-mediated deletion of Bcl-xL in lung adenocarcinoma cell lines. (B) BH3 profile of four Bcl-xL knockout lung adenocarcinoma cell lines showing that Bcl-xL deletion increases mitochondrial apoptotic priming. (C) Priming measured by BIM peptide is significantly increased in four Bcl-xL knockout lung adenocarcinoma cell lines. (D) Bcl-xL deletion is sufficient to switch cell fate of p53-restored lung adenocarcinoma cells from cell cycle arrest to apoptosis. Data shown is from cells harvested 72 h after p53 restoration. (E) Fold-change in the percentage of Annexin V–7-AAD double-positive control or Bcl-xL knockout cells 72 h after p53 restoration. Data in C and E represent the mean ± SEM, n = 3 or more. Statistics were calculated with two-sided Student’s t test: **P < 0.01, ***P < 0.001, ****P < 0.0001; n.s., not significant.