Anticancer effect of icaritin on human lung cancer cells through inducing S phase cell cycle arrest and apoptosis.
10.1007/s11596-014-1305-1
- Author:
Qian ZHENG
1
;
Wei-wei LIU
;
Bin LI
;
Hui-jie CHEN
;
Wen-shan ZHU
;
Guang-xiao YANG
;
Ming-jie CHEN
;
Guang-yuan HE
Author Information
1. The Genetic Engineering International Cooperation Base of Chinese Ministry of Science and Technology, Key Laboratory of Molecular Biophysics of Chinese Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, 430074, China, zhengq0104@163.com.
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents, Phytogenic;
pharmacology;
Apoptosis;
drug effects;
Cell Line, Tumor;
Flavonoids;
pharmacology;
Humans;
Lung Neoplasms;
drug therapy;
metabolism;
pathology;
MAP Kinase Signaling System;
drug effects;
Neoplasm Proteins;
biosynthesis;
Reactive Oxygen Species;
metabolism;
S Phase Cell Cycle Checkpoints;
drug effects
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2014;34(4):497-503
- CountryChina
- Language:English
-
Abstract:
Icaritin, a prenylflavonoid derivative from Epimedium Genus, has been shown to exhibit many pharmacological and biological activities. However, the function and the underlying mechanisms of icaritin in human non-small cell lung cancer have not been fully elucidated. The purpose of this study was to investigate the anticancer effects of icaritin on A549 cells and explore the underlying molecular mechanism. The cell viability after icaritin treatment was tested by MTT assay. The cell cycle distribution, apoptosis and reactive oxygen species (ROS) levels were analyzed by flow cytometry. The mRNA and protein expression levels of the genes involved in proliferation and apoptosis were respectively detected by RT-PCR and Western blotting. The results demonstrated that icaritin induced cell cycle arrest at S phase, and down-regulated the expression levels of S regulatory proteins such as Cyclin A and CDK2. Icaritin also induced cell apoptosis characterized by positive Hoechst 33258 staining, accumulation of the Annexin V-positive cells, increased ROS level and alteration in Bcl-2 family proteins expression. Moreover, icaritin induced sustained phosphorylation of ERK and p38 MAPK. These findings suggested that icaritin might be a new potent inhibitor by inducing S phase arrest and apoptosis in human lung carcinoma A549 cells.