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. 2022 Jan 11;13:245. doi: 10.1038/s41467-021-27921-1

Fig. 10. Knockout of MAPK4 sensitizes MDA-MB-231 cells and xenografts to PI3K inhibition.

Fig. 10

a Soft-agar assays for anchorage-independent growth of wild type (WT) and MAPK4-knockout (KO, clone #3) MDA-MB-231 cells, as well as MAPK4-KO MDA-MB-231 cells with ectopic expression of MAPK4 (KO-MAPK4), in the presence of PI3K inhibitors LY294002, Pictilisib, Alpelisib, or vehicle control (DMSO). Bar: 500 μm. The right panels show quantification (mean ± SEM) of colonies formed under each treatment condition described/numbered in the left panels. Adjusted P values determined by two-way ANOVA followed by Sidak’s multiple comparisons. Data are representative of at least three independent experiments. b The weekly measurement of the growth (sizes) of wild type (WT) and MAPK4-knockout (KO) MDA-MB-231 xenograft tumors with 3-week continuous treatments of Alpelisib (daily oral gavage at 20 mg/kg) or Vehicle. Week 0 indicates the initial time point when measurable xenografts were detected. Arrow indicates beginning of Alpelisib treatment one week after tumor detection. c Xenograft tumors and tumor weights at collection. Xenograft tumor data are representative of two independent experiments. Data are mean ± SEM. P values determined by unpaired two-tailed Student’s t test. Source data are provided as a Source data file.