Figure 1.

The proposed mechanism of urokinase-type plasminogen activator receptor (uPAR)-targeted β-E liposomes combined with cisplatin (DDP) for the treatment of bladder cancer. (A) The uPAR was highly expressed in tumor cells, angiogenic endothelial cells, stromal fibroblasts, and macrophages. The binding of ATF₂₄ peptide-modified liposomes to stromal fibroblasts, macrophages, and tumor cells enhanced the retention of liposomes in the tumor microenvironment and tumor tissues. Receptor-mediated internalization of nanoparticle drug carriers increased cellular drug delivery and therapeutic effects. (B) The combination of ATF₂₄-PEG-Lipo-β-E and DDP significantly inhibited KU-19-19 cell proliferation and promoted cell apoptosis, which were associated with the caspase-dependent pathway and the Cdc25C/Cdc2/cyclin B1 signaling pathway.