Fig. 1

Desloratadine significantly inhibits the proliferation and growth of HCC cells in vitro and in vivo. a Diagram showing the procedure for screening an FDA-approved drug library for antitumor drugs. b CCK-8 assays showing cell viability upon compound treatment (20 µM, 48 h). c Chemical structure of desloratadine. d Huh7 and HepG2 cells were treated with different concentrations of desloratadine or vehicle (DMSO), and cell proliferation was evaluated by a CCK-8 assay. e The effect of desloratadine on colony formation was monitored. f Cells were treated with DMSO or desloratadine for 48 h. The apoptosis rate was analyzed by flow cytometry. g Huh7 and HepG2 cells were treated with DMSO or desloratadine for 48 h, and the levels of cleaved PARP and cleaved caspase-3 were determined by Western blot analysis. β-actin served as the internal control. h Cells were treated with DMSO or desloratadine for 24 h, and the cell cycle distribution was analyzed by flow cytometry. i The level of p-CDK1 and cyclin B1 were analyzed by Western blot. β-actin served as the internal control. j Migration and invasion capacities of Huh7 and HepG2 cells with/without desloratadine treatment (4 and 6 µg/ml in Huh7 cells and 6 and 8 µg/ml in HepG2 cells) were compared using Transwell assays. k Nude mice bearing Huh7- or HepG2-derived xenografts were orally administered desloratadine (15 mg/kg or 45 mg/kg) or vehicle once every two days (n = 6 mice per group). Representative images of the tumors and tumor growth curves showed that desloratadine significantly suppressed the growth of xenograft tumors. l Representative images of Ki67 staining in tumor tissue. Bars, SDs; *p < 0.05; **p < 0.01, ***p < 0.001, and n.s., no significance