Inhibition of Jurkat T Cell Growth by N-farnesyl-norcantharimide Through Up-regulation of Tumor Suppressor Genes and Down-regulation of Genes for Steroid Biosynthesis, Metabolic Pathways and Fatty Acid Metabolism
| Autor: | Jin-Yi Wu, Cheng-Deng Kuo, Hui-Fen Liao, Yu-Jen Chen, Jui-Feng Lin, En-Tung Tsai, Fang-Yu Yang |
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| Rok vydání: | 2020 |
| Předmět: | |
| Zdroj: | Anticancer Research. 40:2675-2685 |
| ISSN: | 1791-7530 0250-7005 |
| DOI: | 10.21873/anticanres.14238 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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