fig9

From: FGFR1 overexpression promotes resistance to PI3K inhibitor alpelisib in luminal breast cancer cells through receptor tyrosine kinase signaling-mediated activation of the estrogen receptor

FGFR1 overexpression promotes resistance to PI3K inhibitor alpelisib in luminal breast cancer cells through receptor tyrosine kinase signaling-mediated activation of the estrogen receptor

Figure 9. FGFR1 knockdown reverses alpelisib resistance in T47D/FGFR1 cells. (A) Immunoblot analysis of FGFR1 protein levels in T47D/FGFR1 (TF) cells following transfection with FGFR1-targeting siRNA (TF/siFGFR1) or scramble control (TF/siC); (B) CCK-8 measurement of the dose-response curves of TF/siC and TF/siFGFR1 cells followed by IC₅₀ calculation; (C) Comparison of the IC₅₀ values between the two groups analyzed with Welch’s t-test; (D and E) Clonogenic assays of TF/siC and TF/siFGFR1 cells. Twenty-four h after siRNA transfection, the cells were reseeded and treated with alpelisib at indicated concentrations. Quantified colony formation efficiencies were analyzed with a two-way ANOVA test. ^**P < 0.01.