Hyperforin suppresses tumor growth and NF-ĸB-mediated anti-apoptotic and invasive potential of non-small cell lung cancer

Background/Aim: Previous studies have indicated that hyperforin inhibits tumor growth of hepatocellular carcinoma. However, the anticancer effects of hyperforin in non-small cell lung cancer (NSCLC) are ambiguous. The aim of the present study was to investigate the anticancer effect of hyperforin in NSCLC. NSCLC CL1-5-F4 cells were treated with different concentrations of hyperforin or NF-ĸB inhibitor (QNZ) for different time periods. Materials and Methods: Change of cell viability, NF-ĸB activation, apoptotic signaling pathways, expression of anti-apoptotic proteins, and cell invasion were detected using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, NF-ĸB reporter gene assay, flow cytometry, western blotting, and cell invasion assay. Results: The results demonstrated that hyperforin significantly promotes extrinsic and intrinsic apoptotic pathways, and inhibits cell viability and NF-ĸB activation. In addition, results also indicated that blockage of NF-ĸB activation reduces the levels of anti-apoptotic proteins and cell invasion in CL1-5-F4 cells. Conclusion: These results suggested hyperforin induces apoptosis and inhibits NF-ĸB-modulated anti-apoptotic and invasive potential in NSCLC.