fig1

Figure 1. FGFR1 overexpression promotes resistance to alpelisib in MCF-7 cells. (A) Protein levels of FGFR1 in MCF7/C and MCF7/FGFR1 cells detected by Western blotting; (B) Alpelisib-induced inhibition of MCF7/C and MCF7/FGFR1 cells assessed with the CCK-8 assay. Cells were treated with alpelisib at indicated concentrations for five days, and survival fractions were determined. IC₅₀ values were calculated using GraphPad Prism software; (C) IC₅₀ values based on three experiments were analyzed with Welch’s t-test. ^**P < 0.01; (D) Clonogenic assays of MCF7/C and MCF7/FGFR1 cells treated with alpelisib. Cells were seeded at 600 cells/well and treated with alpelisib for two weeks, followed by crystal violet staining and quantification; (E) Representative images from the clonogenic assay as described in (D); (F) Cell cycle analysis of MCF7/C and MCF7/FGFR1 cells treated with 0.3 μM alpelisib (Alp) for 24 h, followed by flow cytometry analysis in triplicate. Percentages of cells in the S phase are indicated for each sample; (G) Decrease in S-phase cells between alpelisib-treated MCF7/C and MCF7/FGFR1 cells as assessed in (F). The percentage of S-phase cells in drug-treated samples was normalized by dividing by the percentage of S-phase cells in the corresponding untreated cell line. ^**P < 0.01.