Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/Akt pathway

doi:10.1016/j.phytochem.2021.112901

中山醫學大學機構典藏 CSMUIR > 中山醫學大學研究成果 > 期刊論文 > Item 310902500/23961

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题名:	Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/Akt pathway
作者:	Dong, JR;Chang, WW;Chen, SM
关键词:	Cancer cell biology;Sequiterpene alcohol;ATM/Akt;Nerolidol;Reactive oxygen species;G1 cell cycle arrest;DNA damage
日期:	2021
上传时间:	2022-08-05T09:45:37Z (UTC)
出版者:	PERGAMON-ELSEVIER SCIENCE LTD
ISSN:	0031-9422
摘要:	Nerolidol (3,7,11-trimethyl-1,6,10-dodecatrien-3-ol), a sesquiterpene alcohol present in aromatic essential oils of numerous plants, has been reported to possess anticancer activity. The potential therapeutic effect of nerolidol on uterine fibroids (UF), the most common benign tumor of the uterus worldwide, is unknown. In this study, we examined the anti-UF potential of nerolidol in ELT3 cells, a rat leiomyoma cell line widely used as an in vitro model, to identify the potential therapeutic agents for UF. We observed that treatment with cis- or trans-nerolidol inhibited cell proliferation in a dose-dependent manner and induced cell cycle arrest in the G1 phase, which was accompanied by reduction in Akt phosphorylation and downregulation of cyclin D1, cyclin-dependent kinase 4 (CDK4), and CDK6 protein expression. The proliferation-inhibiting activity of nerolidol correlated with the generation of intracellular reactive oxygen species (ROS), which was suppressed by N-acetyl-1-cysteine, a ROS inhibitor. Nerolidol treatment also increased the percentage of cells for which tail moment could be calculated using an alkaline comet assay, and induced p-gamma H2AX(ser139) expression, which indicated induction of DNA damage. We also observed downregulation of ATM and its phosphorylation after nerolidol treatment; furthermore, treatment with KU-55933, an ATM kinase inhibitor, mimicked the inhibitory effects of nemlidol treatment on cell proliferation and Akt phosphorylation. In conclusion, nerolidol displayed anti-UF activity in a leiomyoma cell model via ROS-induced DNA damage and G1 phase cell cycle arrest by inhibiting the expression and activation of the ATM/Akt pathway. Our data suggests that nerolidol is a potential therapeutic agent for UF.
URI:	http://dx.doi.org/10.1016/j.phytochem.2021.112901 https://www.webofscience.com/wos/woscc/full-record/WOS:000696931700001 https://ir.csmu.edu.tw:8080/handle/310902500/23961
關聯:	PHYTOCHEMISTRY ,2021,v191
显示于类别:	[中山醫學大學研究成果] 期刊論文

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