In the present study, we hypothesized that treatment of bladder cancer cells with cisplatin would induce upregulation of HOTAIR, resulting in increases in pro-inflammatory cytokine expression and subsequent cancer cachexia, and that this process is mediated, at least in part, through the EGFR-ProT-NF-κB-HOTAIR signaling axis. This evidence concerns the gene NFKB1 and urinary bladder carcinoma.