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Fig. 3 | Cell & Bioscience

Fig. 3

From: Anti-metastatic effect of GV1001 on prostate cancer cells; roles of GnRHR-mediated Gαs-cAMP pathway and AR-YAP1 axis

Fig. 3

GV1001-induced AR activation in LNCaP cells. A Time-dependent AR phosphorylation (Ser-81) by dihydrotestosterone (DHT, 100 nM) or GV1001 (10 μM) in LNCaP cells. All of the results were confirmed by multiple experiments. B Total AR expression and AR phosphorylation in LNCaP cells treated with GV1001 (0.1–10 μM) for 24 h. C Effect of GV1001 on ARE-reporter activity. LNCaP cells were transiently transfected with ARE-luciferase plasmid (1 μg/ml) and the cells were exposed to DHT (100 nM) or GV1001 (0.1–10 μM) for 24 h. Luciferase activity was determined to assess ARE responsiveness. Data represent means ± SD (n = 6, **P < 0.01 vs vehicle-treated control). D An additive increase in ARE-reporter activity by GV1001 and DHT. GV1001 (0.1–10 μM) was simultaneously treated with dihydrotestosterone (100 nM) in LNCaP cells for 24 h. Data represent means ± SD (n = 8, **P < 0.01 vs vehicle-treated control, #P < 0.05 vs DHT-treated group). E Expression and phosphorylation of AR by GnRH analogs. LNCaP cells were treated with GnRH (0.1–10 μM) or LA (1–100 nM) for 24 h. F Inhibitory effect of GV1001 on flutamide-stimulated LNCaP cell migration. LNCaP cells were treated with flutamide (1 μM) and GV1001 (10 μM) for 24 h. Migratory cell numbers were determined by the IncuCyte ZOOM live-cell analysis system. Data represent means ± SD (n = 4, **P < 0.01 vs vehicle-treated control, #P < 0.05 vs flutamide-treated group)

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