Fig. 7: Antitumor effect of AdipoRon.

a Effect of oral administration of AdipoRon on the growth of subcutaneous MIAPaCa-2 tumours. Twelve days after subcutaneous implantation of MIAPaCa-2 cells (1 × 10⁶ cells), vehicle alone or AdipoRon (60 mg/kg) were orally administered every other day (n = 6 per group). b Tumour weight (n = 6 per group). c Body weight (n = 6 per group). d Proliferation of MIAPaCa-2 cells in tumours. Tissue sections were stained for Ki67. The percentage of Ki67-positive cells (n = 14 and 15 for vehicle and AdipoRon group, respectively) is shown on the right. Nuclei were also stained with DAPI. Bars: 100 μm. e Tumour angiogenesis. Tissue sections were stained for CD31. Nuclei were also stained with DAPI. The vessel density (n = 10 and 14 for vehicle and AdipoRon group, respectively) is shown on the right. Bars: 100 μm. f, g Viability of patient-derived pancreatic cancer cells. Representative images of staining with FITC-labelled anti-EpCAM antibody and PI (f). White and yellow arrowheads represent EpCAM⁻PI⁺ and EpCAM⁺PI⁺ cells, respectively. Bars: 100 μm. The percentage of EpCAM⁺PI⁺ cells (g). Bar: 50 μm. h Effect of MitoTEMPO on AdipoRon-induced cell death of pancreatic cancer cells derived from patients. The cells were pre-treated with 10 μM MitoTEMPO for 1 h and then treated with 100 μM AdipoRon in the absence or presence of 10 μM MitoTEMPO for 40 h. For a–e and h, error bars represent standard deviation. *P < 0.05, **P < 0.01, ***P < 0.001 by Student’s t-test or ANOVA test