fig3

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 3. FGFR1 knockdown restores alpelisib sensitivity in FGFR1-overexpressing MCF-7 cells. (A) Immunoblot analysis of FGFR1 protein levels in MCF-7/FGFR1 (MF) cells following transient transfection with FGFR1-targeting siRNA (MF/siFGFR1) or scramble control (MF/siC); (B) Dose-response curves of alpelisib treatment in MF cells with or without FGFR1 knockdown, demonstrating a significant reduction in IC50 upon alpelisib treatment; (C) The statistical differences in IC50 values between the two groups were analyzed using Welch’s t-test; (D and E) Clonogenic survival assays showing colony formation efficiency of MF cells treated with indicated concentrations of alpelisib (0.03-0.3 µM) following FGFR1 knockdown. Data represent triplicate measurements analyzed by two-way ANOVA. **P < 0.01.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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