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. Author manuscript; available in PMC: 2018 Jun 15.
Published in final edited form as: Cancer Res. 2017 Apr 20;77(12):3144–3150. doi: 10.1158/0008-5472.CAN-16-0708

Figure 3.

Figure 3

PR3 activates RAGE-mediated MAP kinase phosphorylation. Where indicated, tumor cells were incubated in serum-free medium with 1 μg/mL PR3 for 30 min at 37°C prior to fixation. A, PC3/Fl-RAGE cells treated with PR3 were subjected to immunofluorescence with antibodies against the extracellular RAGE domain (green), p44/42 MAP kinase (red) or phosphorylated JNK1 (pJNK, red). Nuclei are stained blue. B, PC3/Fl-RAGE (top) or PC3/Nt-RAGE (bottom) cells with (right) or without (left) PR3 treatment and subjected to anti-pJNK immunofluorescence (red). Scale bar, 50 μm. C, RAGE/PR3 interaction induces tumor cell motility. Migration of PC3, PC3/Fl-RAGE, PC3/Nt-RAGE, and DU145 cells was evaluated in a transwell assay in the presence of PR3 and JNK inhibitor II, or in control conditions. The numbers of migrated cells are shown as mean ± SEM from three independent experiments. *P<0.05, ** P<0.01, *** P<0.001.