JNK Inactivation Induces Polyploidy and Drug-Resistance in Coronarin D-Treated Osteosarcoma Cells

Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry
Chang-Te HsuTai-Shan Shen

Abstract

Inhibition of proliferating cells is a critical strategy for cancer therapy. In this study, we demonstrated that coronarin D, a natural component extracted from the rhizomes of Hedychium coronarium, significantly suppressed the proliferation of osteosarcoma cells. The treatment with coronarin D resulted in the activation of caspase-3 and apoptosis. This treatment induced the accumulation of cyclin B1 and DNA condensation indicating the treated osteosarcoma cells were arrested in mitotic phase. Furthermore, the treatment with coronarin D increased the levels of phosphorylated c-Jun NH2-terminal kinase (JNK) in human osteosarcoma cells. Pretreatment with JNK inhibitor blocked the accumulation of cyclin B1 and DNA condensation, resulting the accumulation of tetraploid cells in coronarin D-treated osteosarcoma HOS cells, indicating JNK inactivation blocked the mitotic entry and arrested cells in the 4 N state. After adaptation, the arrested tetraploid cells continued to duplicate their DNA resulting in polyploidy. Interestingly, when the arrested mitotic cells induced by coronarin D were treated with JNK inhibitor, the accumulated cyclin B1 and DNA condensation were immediately eliminated. These arrested 4 N cells loss the ability ...Continue Reading

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Citations

Feb 8, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Roberto Fabiani
Oct 14, 2018·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Luna GeJinxiang Han
Apr 12, 2021·Seminars in Cancer Biology·Jing ZhangXinzhe Liu

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Methods Mentioned

BETA
flow cytometry
electrophoresis

Software Mentioned

Excel
GraphPad Prism
GraphPad

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