ERK/GSK3β signaling is involved in atractylenolide I-induced apoptosis and cell cycle arrest in melanoma cells

doi:10.3892/or.2015.4111

	ERK/GSK3β signaling is involved in atractylenolide I-induced apoptosis and cell cycle arrest in melanoma cells
	Ye, Yan 2; Chao, Xiao-Juan 2; Wu, Jin-Feng 2; Cheng, Brian Chi-Yan 2; Su, Tao 2; Fu, Xiu-Qiong 2; Li, Ting 2; Guo, Hui 2; Tse, Anfernee Kai-Wing 2; Kwan, Hiu-Yee 2
刊名	Oncology reports
	2015-09
卷号	34 期号:3 页码:1543-8
ISSN号	1791-2431
DOI	10.3892/or.2015.4111
文献子类	Article
英文摘要	Novel agents need to be developed to overcome the limitations of the current melanoma therapeutics. Atractylenolide I (AT-I) is a sesquiterpene compound isolated from atractylodis macrocephalae rhizoma. Previous findings demonstrated that AT-I exhibited cytotoxic action in melanoma cells. However, the molecular mechanisms of AT‑1's anti-melanoma properties remain to be elucidated. In the present study, the cell cycle-arrest and apoptosis-promoting effects as well as the ERK/GSK3β signaling-related mechanism of action of AT-I were examined. B16 melanoma cells were treated with various concentrations of AT-1 (50, 75 and 100 µM) for 48 or 72 h. Cell cycle and apoptosis were analyzed by flow cytometry. Protein expression levels were detected by western blot analysis. AT-I treatment induced G1 phase arrest, which was accompanied by increased p21 and decreased CDK2 protein expression levels. Apoptosis was observed after AT-I treatment for 72 h, which was accompanied by activated caspase‑3 and ‑8. AT-I treatment significantly decreased phospho-ERK, phospho-GSK3β, c-Jun and increased p53 protein expression levels. Lithium chloride (LiCl, 5 mM), a GSK3β inhibitor, treatment alone did not increase the apoptosis of B16 cells, while pretreatment with LiCl markedly reversed AT-I-induced apoptosis. Additionally, AT-I-induced G1 phase arrest was partially reversed by LiCl pretreatment. In conclusion, ERK/GSK3β signaling was involved in the apoptotic and G1 phase arrest effects of AT-I in melanoma cells.
语种	英语
内容类型	期刊论文
源URL	[http://119.78.100.183/handle/2S10ELR8/266521]
专题	中国科学院上海药物研究所
作者单位	1.Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China 2.Center for Cancer and Inflammation Research, School of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong, P.R. China;
推荐引用方式 GB/T 7714	Ye, Yan,Chao, Xiao-Juan,Wu, Jin-Feng,et al. ERK/GSK3β signaling is involved in atractylenolide I-induced apoptosis and cell cycle arrest in melanoma cells[J]. Oncology reports,2015,34(3):1543-8.
APA	Ye, Yan.,Chao, Xiao-Juan.,Wu, Jin-Feng.,Cheng, Brian Chi-Yan.,Su, Tao.,...&Yu, Zhi-Ling.(2015).ERK/GSK3β signaling is involved in atractylenolide I-induced apoptosis and cell cycle arrest in melanoma cells.Oncology reports,34(3),1543-8.
MLA	Ye, Yan,et al."ERK/GSK3β signaling is involved in atractylenolide I-induced apoptosis and cell cycle arrest in melanoma cells".Oncology reports 34.3(2015):1543-8.