Jin-Yi Wu1, En-Tung Tsai2, Fang-Yu Yang1, Jui-Feng Lin3,4, Hui-Fen Liao5, Yu-Jen Chen6, Cheng-Deng Kuo7,8,9. 1. Department of Microbiology, Immunology and Biopharmaceutics, College of Life Sciences, National Chiayi University, Chiayi, Taiwan, R.O.C. 2. Department of Medical Research, Taipei Veterans General Hospital, Taipei, Taiwan, R.O.C. 3. Division of Neurosurgery, Department of Surgery, Mackay Memorial Hospital, Taipei, Taiwan, R.O.C. 4. Institute of Traditional Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwan, R.O.C. 5. Department of Biochemical Science and Technology, National Chiayi University, Chiayi, Taiwan, R.O.C. 6. Department of Radiation Oncology, Mackay Memorial Hospital, Taipei, Taiwan, R.O.C. 7. Department of Medical Research, Taipei Veterans General Hospital, Taipei, Taiwan, R.O.C. cdkuo23@gmail.com. 8. Division of Chest Medicine, Department of Internal Medicine, Changhua Christian Hospital, Changhua, Taiwan, R.O.C. 9. Tanyu Research Laboratory, Taipei, Taiwan, R.O.C.
Abstract
BACKGROUND/AIM: To evaluate the anti-cancer mechanism of N-Farnesyl-norcantharimide (NC15). MATERIALS AND METHODS: The viability of NC15-treated human leukemic Jurkat T (JKT) cells was assessed using the Kit-8 cell counting method. Flow cytometry analysis, human apoptosis antibody array assay, and whole genome sequencing were adopted to investigate the mechanism underlying the anti-cancer activity of NC15 in JKT cells. RESULTS: The growth inhibition rates of NC15 in JKT cells were about 80% and 95% after treatment with 8 μmol/l NC15 for 24 and 48 h, respectively. The percentages of NC15-treated JKT cells in the sub-G1 phase at 24 and 48 h were 22.0% and 34.3%, respectively, in contrast to the 1.5% in the control. Next-generation sequencing showed that many tumor suppressor genes (TSG) were up-regulated, while many genes associated with steroid biosynthesis, metabolic pathways, and fatty acid metabolism were down-regulated. CONCLUSION: NC15 can reduce the cell viability and increase the percentage of JKT cells in the sub-G1 phase by up-regulating TSG and related genes, and down-regulating the genes for steroid biosynthesis, metabolic pathways and fatty acid metabolism, instead of through apoptosis. Copyright
BACKGROUND/AIM: To evaluate the anti-cancer mechanism of N-Farnesyl-norcantharimide (NC15). MATERIALS AND METHODS: The viability of NC15-treated humanleukemic Jurkat T (JKT) cells was assessed using the Kit-8 cell counting method. Flow cytometry analysis, human apoptosis antibody array assay, and whole genome sequencing were adopted to investigate the mechanism underlying the anti-cancer activity of NC15 in JKT cells. RESULTS: The growth inhibition rates of NC15 in JKT cells were about 80% and 95% after treatment with 8 μmol/l NC15 for 24 and 48 h, respectively. The percentages of NC15-treated JKT cells in the sub-G1 phase at 24 and 48 h were 22.0% and 34.3%, respectively, in contrast to the 1.5% in the control. Next-generation sequencing showed that many tumor suppressor genes (TSG) were up-regulated, while many genes associated with steroid biosynthesis, metabolic pathways, and fatty acid metabolism were down-regulated. CONCLUSION:NC15 can reduce the cell viability and increase the percentage of JKT cells in the sub-G1 phase by up-regulating TSG and related genes, and down-regulating the genes for steroid biosynthesis, metabolic pathways and fatty acid metabolism, instead of through apoptosis. Copyright