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. 2013 Jun 18;109(1):50–59. doi: 10.1038/bjc.2013.240

Figure 2.

Figure 2

Mechanism of regulation of FGFR3 in hypoxia. (A) RT4 and (B) RT112 cells were cultured in normoxia (N), 0.1% O2 (H) or in normoxia and treated with DMOG for 24 h, and whole cell lysates were probed for FGFR3, HIF-1α and ACTB. Quantification of representative western blots are shown. (C) Expression of FGFR3 mRNA in RT4 cells cultured in normoxia (N), 0.1% O2 (H) or in normoxia and treated with DMOG for 24 h. (D) Expression of FGFR3 protein in RT4 cells cultured in normoxia (N) or 0.1% O2 (H) for 24 h after transfection with scramble (Scr) siRNA or siRNA against HIF-1α or HIF-2α. Quantification of a representative western blot is shown. (E) Expression of FGFR3 protein in RT4 cells cultured in normoxia (N) or 0.1% O2 (H) and treated with the transcription inhibitor actinomycin D (ActD). Quantification of a representative western blot is shown. (F) Luciferase induction from an FGFR3 promoter reporter construct transfected into RT112 cells cultured for 24 h in normoxia (N), 0.1% O2 (H) or in normoxia and treated with 1 mℳ DMOG. (A and D) data are representative of two independent experiments, (B and E) data are representative of one experiment, (C and F). Data are mean and s.e.m. of the mean of three independent experiments. *P<0.05, **P<0.01, ***P<0.001.