Fig. 7: PRR11-amplified breast cancer cells are dependent on the PI3K pathway.

a PIK3CA dependency scores of 57 breast cancer cell lines were plotted against PRR11 copy number (DEMETER2 V5 dataset; Pearson correlation). b Sensitivity of 27 breast cancer cell lines to pictilisib and taselisib was plotted against PRR11 copy number (PRISM Repurposing 19Q3 dataset; Pearson correlation). Y-axis shows the log 2 cell fraction as per the relative barcode abundance following drug treatment. c Pictilisib sensitivity score of 26 breast cancer cell lines in the LINCS MGH/Sanger dataset (n = 22 and 4 for non-amplification and amplification group, respectively). Data represent the mean ± SD (two-tailed unpaired t-tests). d, e Alpelisib (d) and taselisib (e) GR₅₀ of MDA-MB-134VI and MDA-MB-175VII cells transduced with pLX302-LacZ or pLX302-PRR11 were calculated using the GR metrics calculator. Cell numbers counted at day 0 and day 6 were used as the input data. Data represent the mean ± SD of three replicates (two-tailed unpaired t-tests). f Low density monolayers of MDA-MB-134VI pLX302-LacZ and -PRR11 cells were grown in estrogen (E2)-free medium. After 14 days, cell monolayers were stained with crystal violet. Data represent the mean ± SD of three replicates (two-tailed unpaired t-tests). g, h Low density monolayers of MDA-MB-175VII and MDA-MB-134VI cells transduced with pLX302-PRR11 or pLX302-LacZ were treated ± 1 µM alpelisib (g) or ± 1 µM taselisib (h) in estrogen-free medium. After 14 days, cell monolayers were stained with crystal violet. Data represent the mean ± SD of three replicates (two-tailed unpaired t-tests). Source data are provided as a Source data file.