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[Preprint]. 2025 Jul 10:2025.07.06.663368. [Version 1] doi: 10.1101/2025.07.06.663368

Fig. 5: The genetic determinant of drug sensitivity is p53 transcription activity dependent.

Fig. 5:

(A) Cell cycle assay using flow cytometry with Propidium iodide (PI) staining after treatment of exatecan at 100nM at indicated timepoint on organoids derived from H (Top) and H53fl/fl (bottom) mice. (B) Western blotting of KAP1, p21, phosphor-KAP1, phospho-CHK1, total CHK1, phospho-CHK2, total CHK2, phospho-HER2, total HER2, phospho-H2Ax, phospho-caspase3 and GAPDH from exatecan-treated H53 null organoid cells in Figure 3A. (C) The cell cycle profile was assayed by FACS analysis with PI staining on the breast tumor organoids isolated from H53wt/fl, H53fl/fl, and H53fl/172 mice. (D) The percentage of cells in each cell cycle phases was detected by BrdU-PI co-staining from tumor organoids cells isolated from Hwt/172, H53fl/fl, and H53fl/172 mice. Error bars are based on triplicated technical replicates. (E) Cell cycle phase analysis based on the FACS result from figure 5D. Error bars are based on triplicate of technical repeats. (F) Quantification of the percentage of apoptotic organoid cells. Apoptosis assay using FACS by annexin V staining after 3 days of treatment of 100nM exatecan on organoids derived from H, HP, and H53fl/fl group mice. Error bars are based on triplicate of technical repeats.