fig6

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 6. ERα phosphorylation/activation in FGFR1-driven alpelisib resistance and sensitization by combination therapy. (A) Sustained ERα phosphorylation in alpelisib (Alp)-treated MCF7/FGFR1 cells. Cells of both sublines were treated with alpelisib at the indicated concentrations for 24 h. Protein levels of p-ERα/S118, p-ERα/S167, ERα, and the internal control GAPDH were detected by Western blotting; (B) Combination of alpelisib with AZD4547 enhances inhibition of ERα phosphorylation/activation. MCF7/C and MCF7/FGFR1 cells were treated with 2 μM alpelisib (Alp), 6 μM AZD4547 (AZD), or the combination for 24 h, followed by Western blot analysis of p-ERα/S118, p-ERα/S167, ERα, and GAPDH in the indicated groups.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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