2β, 3β, 23-trihydroxy-urs-12-ene-28-olic acid (TUA) isolated from Actinidia chinensis Radix inhibits NCI-H460 cell proliferation by decreasing NF-κB expression

• TUA, which isolated from Actinidia chinensis Radix, was a natural ursolic compound.
• The research was carried out to investigate the apoptotic mechanism of TUA.
• TUA induced apoptosis via inhibition of NF-κB expression level in NCI-H460 cells.
• TUA will be a potent anticancer candidate for lung cancer treatment in future.

A natural ursolic compound, 2β, 3β, 23-trihydroxy-urs-12-ene-28-olic acid (TUA) was isolated from the root of Actinidia chinensis Planch (A. chinensis Radix). Since a large number of triterpenoid compound has marked anticancer effects toward various types of cancer cell lines in vitro, this study was carried out to investigate the anticancer effect of TUA in non-small cell lung cancer cells (NSCLCCs) and the underlying apoptotic mechanism of TUA was examined in NCI-H460 cell lines. Cell proliferation, apoptosis and cell cycle were measured using a cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The activity of transcription factor NF-κB was determined by EMSA method. The expression of apoptosis- and proliferation-related proteins was determined by western blotting. The effect of TUA on NF-κB mRNA expression in NCI-H460 cells was detected by RT-PCR. TUA significantly suppressed the viability of NCI-H460 cells. Also, TUA significantly increased the sub G1 population by cell cycle analysis and in a concentration dependent manner in NCI-H460 cells. Such an effect was accompanied by p65 (NF-κB subunit) inactivation by an inhibition of IκBα phosphorylation, and by inhibition of p65 mRNA expressions. Consistently Overall, our findings suggest that TUA induces apoptosis via inhibition of NF-κB (p65) expression level and activation of IκBα in NCI-H460 cells as a potent anticancer candidate for lung cancer treatment.