Gambogenic acid suppresses bladder cancer cells growth and metastasis by regulating NF-κB signaling.

Abstract

Gambogenic acid (GNA) is one of the main active components of Gamboge, and its anticancer role has been reported in some cancers. The study was to investigate the inhibitory effects of GNA on the proliferation and metastasis of bladder cancer (BC) cells and its potential regulatory mechanisms. BC cell lines (BIU-87 cells, T24 cells, and J82 cells) were treated with different doses of GNA for different time, and then the effects of GNA on BC cell were examined in vitro using CCK-8 assay, apoptosis assays, and Transwell tests. NF-κB signaling activity was detected by the NF-κB p65 luciferase reporter assay. Western blot was used to detect the expressions of cIAP2, XIAP, Survivin, and p65. GNA inhibited the viability of BC cells in vitro in a dose- and time-dependent manner and facilitated apoptosis of BC cells. Moreover, GNA could remarkably impede the migration and invasion abilities of BC cells. In terms of mechanism, GNA administration reduced the activity of NF-κB signaling and down-regulated the expressions of p65, survivin, XIAP, and cIAP2. GNA blocks the growth and metastasis of BC cells via inhibiting the NF-κB signal transduction pathway.