fig4

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 4. The combination of FGFR1-targeting AZD4547 with alpelisib induces significant synergistic inhibitory effects. (A) and (B) Combination index (CI) of MCF7/C (A) and MCF7/FGFR1 (B) cells treated with alpelisib (Alp) and AZD4547 in various combinations. Cells were treated with the drugs at indicated concentrations for 5 days, followed by CCK-8 assays. CI values were calculated using CompuSyn software according to the Chou-Talalay method. Only CI values corresponding to a fractional effect (FA) greater than 0.5 were presented; (C) and (D) Clonogenic assays of MCF7/C and MCF7/FGFR1 cells treated with alpelisib (Alp) or AZD4547 (AZD), alone or in combination. Cells were treated with 0.3 μM alpelisib, 3 μM AZD4547, or the combination for 2 weeks, followed by crystal violet staining; (C) Representative images of the assays; (D) Quantification of colony numbers based on triplicate experiments, displayed as a bar graph; (E) Cell cycle analysis of MCF7/C and MCF7/FGFR1 cells treated with alpelisib (Alp) or AZD4547 (AZD), alone or in combination. Cells were treated with 1 μM alpelisib, 10 μM AZD4547, or the combination for 24 h, followed by flow cytometry analysis in triplicate. **P < 0.01 indicates significant differences in S-phase cell populations between the indicated groups.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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