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. 2023 Jul 3;14(11):1946–1955. doi: 10.7150/jca.84170

Figure 2.

Figure 2

ER stress induces cancer cell apoptosis via TAp73α. (A-B) HCT116p53-/- cells were treated with or without ER stress inducers (BFA and TM) at the indicated concentrations for 24 h (A) or a concentration of 2 μg/mL for different times (B) and then subjected to western blot analysis. (C-F) p53 null HCT116 cells stably expressing shC or shp73 were treated with or without ER stress inducers for 24 h, and then subjected to western blot analysis, in which cleaved-caspase 3 (C-caspase3) were be quantified based on total-caspase 3 (T-caspase3) or GAPDH (C), MTS assay (D) and FACS analysis (E), and quantitative analysis of FACS data from three independent experiments (F). (G) Whole cell lysates derived from HCT116p53+/+, HCT116p53-/- cells and HEK-293T cells transiently transfected with TAp73α, TAp73β or ΔNp73α were subjected to western blot analysis. (H-K) HCT116p53-/- stably expressing empty vector (EV) or TAp73α, and then subjected to western blot analysis, in which cleaved-caspase 3 (C-caspase3) were be quantified based on total-caspase 3 (T-caspase3) or GAPDH (H), MTS assay (I) and FACS analysis (J), and quantitative analysis of FACS data from three independent experiments (K). The results are presented as the mean ± SD of three independent experiments; **, P<0.01.