Fig. 3: BAX interaction with BCL-XL dictates sensitivity to BTSA1.2 and Navitoclax combination.
From: Co-targeting of BAX and BCL-XL proteins broadly overcomes resistance to apoptosis in cancer
a BH3-profiling predicts apoptotic blocks correlated with sensitivity to the BTSA1.2 and Navitoclax combination. b–c Western blot analysis of BAX Co-IP in b, NSCLC and c colorectal cell lines. Representative blot from n = 2 independent experiments. d Quantification of co-immunoprecipitated BAX with BCL-XL in cell lines according to the BTSA1.2 and Navitoclax combination activity (corresponding to Fig. 2a–c). Data is the the normalized values obtained from b, c ± SD from n = 2–3 independent experiments e, f, Western blot analysis of BAX IP in e, NSCLC cell line Calu-6 and f, colorectal cell line SW480 after 4 h treatment with BTSA1.2 and Navitoclax. g, h Detection of cleaved Caspase-3 apoptotic marker by western blot analysis in g, NSCLC cell line Calu6 and h, colorectal cell line SW480 after 4 h treatment with BTSA1.2 and Navitoclax. i Dynamic BH3-profiling of solid tumor cell lines treated with vehicle, Navitoclax, BTSA1.2, or the combination. Bar graph represent % of mitochondria depolarization of cancer cells detected by JC-1 upon treatment with BIM-BH3 derived peptide. Data are mean ± SD of three technical replicates from n = 2 independent experiments. j Schematic of sensitive cells to the BTSA1.2 and Navitoclax combination. Western blot data are a representative of at least three independent experiments. Source data are provided as a Source Data file.
