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. 2021 Feb 15;12(2):179. doi: 10.1038/s41419-021-03457-6

Fig. 3. Dinaciclib sensitizes HER2-amplified breast cancer cells to tucatinib and liberates BAK from MCL-1.

Fig. 3

A BT-474 and MDA-MB-453 cells were treated with no drug, 1 μM tucatinib, 100 nM dinaciclib, and their combination for 6 and 12 h, respectively. Whole-cell lysates were prepared, subjected to western blotting and probed for the indicated proteins. B BT-474 cells were treated with increasing concentrations of tucatinib and 100 nM dinaciclib for 24 h and the percentage of viable cells was determined. n = 3; error bars indicate ±SD. C MDA-MB-453 cells were treated with increasing concentrations of tucatinib and 100 nM dinaciclib for 48 h and the percentage of viable cells was determined. n = 3; error bars indicate ±SD. D MCL-1 complexes were immunoprecipitated from MDA-MB-453 cells following 12 h treatment with no drug, 1 μM tucatinib, 100 nM dinaciclib, and their combination. An IgG-matched isotype antibody was served as an immunoprecipitation control. The interaction between MCL-1 and BIM EL/BAK proteins was investigated. For Fig. 3B, C two-tailed Student’s t test was performed; p values were corrected for multiple testing using the Bonferroni method. Differences were considered statistically different if p < 0.05. A p value < 0.05 is indicated by *, p < 0.01 by **, p < 0.001 by ***, and p < 0.0001 by ****. (“No Rx”: No drug).