Cho Seong Hyeok, Kang In-Cheol
Department of Biological Science, College of Natural Science, and BioChip Research Center, Hoseo University, Republic of Korea.
Department of Biological Science, College of Natural Science, and BioChip Research Center, Hoseo University, Republic of Korea; InnoPharmaScreen Inc., Asan 336-795, Republic of Korea.
Biochem Biophys Res Commun. 2018 Apr 6;498(3):431-436. doi: 10.1016/j.bbrc.2018.02.188. Epub 2018 Feb 26.
The goal of this study is to determine the anti-cancer mechanism of Cordycepin in A549 Cisplatin-Resistance (CR) lung cancer cells. Cordycepin inhibited the viability of A549CR cells in a dose-dependent manner. The cell inhibition was due to induction of apoptosis in the cells treated with Cordycepin by activation of caspase -3, -8 and -9 activities. The cell cycle analysis showed that accumulation of Sub G1 was observed in Cordycepin-treated with A549CR lung cancer cells. Based on the data of expression profile analysis of cell signaling proteins using IPS-FPAA, H-Ras was down-regulated in Cordycepin-treated A549CR cells. Collectively, anti-proliferative function of Cordycepin was due to stimulation of the cell apoptosis and the cell cycle arrest via caspases activation and down-regulation of H-Ras.
本研究的目的是确定虫草素对A549顺铂耐药(CR)肺癌细胞的抗癌机制。虫草素以剂量依赖的方式抑制A549CR细胞的活力。细胞抑制是由于虫草素处理的细胞中caspase -3、-8和-9活性的激活诱导了细胞凋亡。细胞周期分析表明,在用虫草素处理的A549CR肺癌细胞中观察到了亚G1期的积累。基于使用IPS-FPAA对细胞信号蛋白表达谱分析的数据,在虫草素处理的A549CR细胞中H-Ras表达下调。总的来说,虫草素的抗增殖功能是由于通过caspases激活和H-Ras下调刺激了细胞凋亡和细胞周期停滞。