Fig. 3: Sildenafil restrains tumor growth of GC through inhibiting PDE5.

A Cell viability of GES-1 cells was analyzed after sildenafil treatment for 24 h and 48 h, with data represented from technical replicates (n = 3). B Total apoptosis rates of GES-1 cells treated with sildenafil for 24 h and 48 h were assessed, with data represented from technical replicates (n = 3). C IC50 analysis of PDE5-knockdown and PDE5-overexpressing GC cells treated with sildenafil was performed after 48 h, with results presented as the mean ± SD from three independent experiments. D Cell viability of PDE5-knockdown and PDE5-overexpressing GC cells was analyzed following 48 h of sildenafil treatment. E Total apoptosis rates of the indicated cells treated with sildenafil for 48 h were assessed. F Inhibitory activity against PDE5A1 in the indicated cells was measured by using PDE5A1 assay kit. G cGMP level was measured by using cGMP ELISA kit. H Cell viability of PDE5-overexpressing GC cells was analyzed following treatment with either sildenafil (150 μM) or 8-Bromo-cGMP (150 μM) for 48 h. I Total apoptosis rates of the indicated cells treated with sildenafil or 8-Bromo-cGMP for 48 h were assessed. J Tumor sizes of xenografts derived from PDE5-overexpressing GC cells treated with sildenafil (15 mg/kg), with DMSO used as the vehicle control. Data are presented from biological replicates (n = 5). K, L Tumor volumes of xenografts were measured on indicated days, and tumor weights were calculated after sildenafil treatment (15 mg/kg). M Tumor burden of xenografts was evaluated. Statistical significance is indicated as follows: ns, P-value > 0.05; *, P-value < 0.05; **, P-value < 0.01; ***, P-value < 0.001.