Fig. 5

Targeting SPOCK1 suppresses prostate cancer growth and metastasis by apigenin (API) in an orthotopic mouse model. a Timeline of the in vivo study design for investigating the effects of SPOCK1 expression on tumor progression and the antitumor activity of API. Male NSG mice were orthotopically injected with luciferase-tagged and SPOCK1-depleted (shSPOCK1) PC-3 M cells or SPOCK1-overexpressing PC-3 cells. After 7 days, mice were treated with API (3 mg/kg, IP) or the vehicle for 6 days/week. Whole body bioluminescence imaging was conducted at different time points after cell-injection in mice. b All mice were sacrificed and dissected at 4 weeks after API treatment, and the luciferase activity was detected every week with an IVIS imaging system (left panel). Quantitative analysis of the Xenogen imaging signal intensity (photons/s) every week (right panel). c Tumors were dissected and photographed after 5 weeks (left panel), and the average tumor weight in each group is given (right panel). Data are presented as the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to the control group. ^# p < 0.05, ^## p < 0.01, ^### p < 0.001 compared to the API-treated group. d-g Representative ex vivo bioluminescence imaging of metastatic sites at the end of this spontaneous metastasis assay. Lungs (d), pancreas (e), liver (f), and bone (g) are major organs for metastasis, and signal intensities of metastatic organs were imaged with bioluminescence at the end of the study, with the mean signal for each group indicated. Data are presented as the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001. h Kaplan-Meier curves and log-rank test of overall survival analysis for indicated tumor-bearing mice treated with API (3 mg/kg, IP) or the vehicle