Acta Pharm. 65 (2015) 463-471


full paper

Original research paper


Induction of cell cycle arrest via the p21, p27–cyclin E,A/Cdk2 pathway in SMMC-7721 hepatoma cells by clioquinol


1 Key Lab of Eco-Textile (Ministry of Education), College of Chemistry, Chemical Engineering and Biotechnology, Donghua University, Shanghai 201620, China

2 Key Laboratory of Organofluorine Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai 200032, China

3 State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai 200237, China

Accepted July 14, 2015


Clioquinol has been shown to have anticancer activity in several carcinoma cells. In this study, we preliminarily examined the effect of clioquinol in human SMMC-7721 hepatoma and QSG-7701 normal hepatic cells. Our results indicated that clioquinol did not significantly affect survival of QSG-7701 cells, whereas it reduced cell viability in a concentration- and time-dependent manner in SMMC-7721 cells. Clioquinol did not trigger autophagy and apoptosis, while it induced cell cycle arrest in the S-phase in SMMC-7721 cells. Additionally, down-regulation of cyclin D1, A2, E1, Cdk2 and up-regulation of p21, p27 were detected after the treatment of clioquinol. The results demonstrated for the first time that clioquinol suppressed cell cycle progression in the S-phase in SMMC-7721 cells via the p21, p27–cyclin E,A/Cdk2 pathway. This suggests that clioquinol may have a therapeutic potential as an anticancer drug for certain malignances.


Keywords: clioquinol, human SMMC-7721 hepatoma cells, cell cycle S-phase arrest, cyclin E/A-Cdk2