Wei-Ting Chen1,2, Ying-Kai Chen3, Song-Shei Lin4, Fei-Ting Hsu5,6,7. 1. Department of Medical Imaging and Radiological Sciences, Central-Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. 2. Department of Psychiatry, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan, R.O.C. 3. Department of Internal Medicine, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan, R.O.C. ccyykk0528@yahoo.com.tw sslin@ctust.edu.tw sakiro920@gmail.com. 4. Department of Medical Imaging and Radiological Sciences, Central-Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. ccyykk0528@yahoo.com.tw sslin@ctust.edu.tw sakiro920@gmail.com. 5. Department of Radiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan, R.O.C. ccyykk0528@yahoo.com.tw sslin@ctust.edu.tw sakiro920@gmail.com. 6. Department of Medical Imaging, Taipei Medical University Hospital, Taipei, Taiwan, R.O.C. 7. Research Center of Translational Imaging, College of Medicine, Taipei Medical University, Taipei, Taiwan, R.O.C.
Abstract
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-κB inhibitor (QNZ) for different time periods. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSION: These results suggested hyperforin induces apoptosis and inhibits NF-κB-modulated anti-apoptotic and invasive potential in NSCLC. Copyright
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. NSCLCCL1-5-F4 cells were treated with different concentrations of hyperforin or NF-κB inhibitor (QNZ) for different time periods. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSION: These results suggested hyperforin induces apoptosis and inhibits NF-κB-modulated anti-apoptotic and invasive potential in NSCLC. Copyright