Fig. 2
From: Aberrant FGFR signaling mediates resistance to CDK4/6 inhibitors in ER+ breast cancer
FGFR1 overexpression confers resistance to fulvestrant and palbociclib. a Tile plot of ER+ breast cancers in TCGA (Cell 2015) with amplification and/or mRNA upregulation of FGFR1, CRKL, HCK, FRK, and FGR. b–d MCF-7eGFP and MCF-7FGFR1 cells were seeded in 6-well plates in full media supplemented with 2 ng/mL FGF2 and treated with vehicle (DMSO), 1 μM fulvestrant, or 1 μM fulvestrant plus 1 μM palbociclib ± 1 μM lucitanib. Drugs and media were replenished every 3 days. After 14 days, monolayers were stained with crystal violet and analyzed as described in Methods. Quantification of the integrated intensity values as fold change relative to vehicle-treated controls are shown (c) (**p < 0.01 vs. controls, Student’s t-test). Cell lysates were subjected to immunoblot analyses with the indicated antibodies (d). e T47DeGFP and T47DFGFR1 cells were seeded in 6-well plates in full media supplemented with 2 ng/mL FGF2 and treated with vehicle (DMSO), 0.5 μM fulvestrant, or 0.5 μM fulvestrant plus 0.5 μM palbociclib ± 1 μM lucitanib. Drugs and media were replenished every 3 days. After 14 days, plates were washed and stained with crystal violet; imaging intensity was quantified by spectrophotometric detection. Quantification of the integrated intensity values as fold change relative to vehicle-treated controls are shown (**p < 0.01 vs. controls, Student’s t-test). Lysates from T47D cells stably transduced with an FGFR1 expression vector were subjected to immunoblot analysis with FGFR1 and actin antibodies (on top-right of the panel)
