Yu-Chang Liu1,2,3, Kuang-Hsuan Lin3, Jung-Hung Hsieh4, Jing-Gung Chung5,6, Zhao-Lin Tan1,6, Fei-Ting Hsu6, Chih-Hung Chiang7,8,9. 1. Department of Medical Imaging and Radiological Sciences, Central Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. 2. Department of Radiation Oncology, Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C. 3. Department of Radiation Oncology, Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C. 4. Department of Urology, Medical Research and Education, Taipei Veterans General Hospital, Yuan-Shan/Su-Ao Branch, Yilan, Taiwan, R.O.C. 5. Department of Biotechnology, Asia University, Taichung, Taiwan, R.O.C. 6. Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, R.O.C. 7. Department of Urology, Medical Research and Education, Taipei Veterans General Hospital, Yuan-Shan/Su-Ao Branch, Yilan, Taiwan, R.O.C. guchiang@gmail.com. 8. Department of Nursing, Cardinal Tien Junior College of Healthcare and Management, New Taipei, Taiwan, R.O.C. 9. Department of Urology, National Taiwan University Hospital, Taipei, Taiwan, R.O.C.
Abstract
BACKGROUND/AIM: Muscle-invasive bladder cancer (MIBC) has long been recognized as a difficult to treat cancer type, thus a new treatment strategy is needed. The major purpose of the present study was to verify the anticancer effect of hyperforin and the mechanism through which it affects tumor cell growth and invasion in bladder cancer in vitro. MATERIALS AND METHODS: Bladder cancer TSGH-8301 cells were treated with different concentrations of hyperforin for different durations of time. The changes in cell viability, production of calcium and reactive oxygen species (ROS), and anti-apoptotic signaling were evaluated using MTT assay, flow cytometry, and western blot analysis. The effect of hyperforin on the expression of nuclear factor-kappaB (NF-ĸB) p65 (Ser276), tumor progression-associated proteins, as well as on cell invasion was investigated using western blotting and cell invasion assay, respectively. RESULTS: Hyperforin significantly induces apoptosis, extrinsic/intrinsic apoptotic signaling, accumulation of cytosol ROS, and calcium signalling. Hyperforin also significantly diminishes the expression of NF-ĸB p65 (Ser276), anti-apoptotic and tumor progression-associated proteins, as well as the cell invasion ability of TSGH-8301 cells. CONCLUSION: Our findings demonstrate that hyperforin triggers apoptosis depending on extrinsic/intrinsic pathways and suppresses NF-ĸB-mediated cell survival as well as the invasive properties of bladder cancer in vitro. Copyright
BACKGROUND/AIM: Muscle-invasive bladder cancer (MIBC) has long been recognized as a difficult to treat cancer type, thus a new treatment strategy is needed. The major purpose of the present study was to verify the anticancer effect of hyperforin and the mechanism through which it affects tumor cell growth and invasion in bladder cancer in vitro. MATERIALS AND METHODS:Bladder cancerTSGH-8301 cells were treated with different concentrations of hyperforin for different durations of time. The changes in cell viability, production of calcium and reactive oxygen species (ROS), and anti-apoptotic signaling were evaluated using MTT assay, flow cytometry, and western blot analysis. The effect of hyperforin on the expression of nuclear factor-kappaB (NF-ĸB) p65 (Ser276), tumor progression-associated proteins, as well as on cell invasion was investigated using western blotting and cell invasion assay, respectively. RESULTS:Hyperforin significantly induces apoptosis, extrinsic/intrinsic apoptotic signaling, accumulation of cytosol ROS, and calcium signalling. Hyperforin also significantly diminishes the expression of NF-ĸB p65 (Ser276), anti-apoptotic and tumor progression-associated proteins, as well as the cell invasion ability of TSGH-8301 cells. CONCLUSION: Our findings demonstrate that hyperforin triggers apoptosis depending on extrinsic/intrinsic pathways and suppresses NF-ĸB-mediated cell survival as well as the invasive properties of bladder cancer in vitro. Copyright
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