hyperforin and Carcinoma--Non-Small-Cell-Lung

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-κB inhibitor (QNZ) for different time periods.. Change of cell viability, NF-κB 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-κB reporter gene assay, flow cytometry, western blotting, and cell invasion assay.. The results demonstrated that hyperforin significantly promotes extrinsic and intrinsic apoptotic pathways, and inhibits cell viability and NF-κB activation. In addition, results also indicated that blockage of NF-κB activation reduces the levels of anti-apoptotic proteins and cell invasion in CL1-5-F4 cells.. These results suggested hyperforin induces apoptosis and inhibits NF-κB-modulated anti-apoptotic and invasive potential in NSCLC.

Topics: Apoptosis; Apoptosis Regulatory Proteins; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Cell Movement; Cell Proliferation; Humans; Lung Neoplasms; Neoplasm Invasiveness; NF-kappa B; Phloroglucinol; Signal Transduction; Terpenes; Tumor Burden