Anticancer potential of corilagin on T24 and TSGH 8301 bladder cancer cells via the activation of apoptosis by the suppression of NF‐κB‐induced P13K/Akt signaling pathway

Abstract

AbstractBladder cancer (BC) is a primary source of malignancy‐associated death, and the mortality rate is high due to its prevalence of metastasis. Corilagin (CLG), a bioactive constituent of numerous medicinal plants, exerts assorted pharmacological actions comprising anti‐cancer, apoptotic, anti‐inflammatory, and hepatoprotective. CLG possesses a substantial anti‐tumor prospective and less noxiousness in normal cells in vitro. However, the molecular mechanisms of CLG on BC cells are not studied well. The current research explored the molecular process intricate in the anticancer and anti‐proliferative actions of CLG on the relocation of BC cells T24 and TSGH 8301. The cytotoxicity, apoptosis, adhesion, and migration of CLG on BC cells T24 and TSGH 8301 were evaluated by MTT assay, DAPI, Rh‐123, cell adhesion, and cell migration assay. The results point out that CLG inhibits the viability, adhesion, movement, incursion, and inflammation, whereas persuades BC cells apoptosis in a concentration‐dependent mode. Besides, CLG treated with T24 and TSGH‐8301 cells subdue inflammatory and PI3K/Akt signaling pathways. CLG is accomplished of impeding BC cell migration, invasion, and metastasis through the repression of the NF‐κB mediated P13K/Akt signaling. Our findings offer a unique vision into the demonstration of the anti‐cancer potential of CLG on BC cells.