Original Article

Telekin suppresses human hepatocellular carcinoma cells in vitro by inducing G2/M phase arrest via the p38 MAPK signaling pathway

Authors: Lin Li, Bei-bei Zheng, Li-sha Ma, Xiao Sun, Juan-juan Chang, Wei-dong Xie, Xia Li
DOI: 10.1038/aps.2014.74


Lin LI1, 2, #, Bei-bei ZHENG1, #, Li-sha MA1, Xiao SUN1, Juan-juan CHANG1, Wei-dong XIE1, Xia LI1, 2, *
1School of Ocean, Shandong University, Weihai 264209, China; 2School of Pharmaceutical Sciences, Shandong University, Ji-nan 250012, China

Aim: Telekin, isolated from the Chinese herb Carpesium divaricatum, has shown anti-proliferation effects against various cancer cells, including hepatocellular carcinoma cells. In this study, we investigated the anti-proliferation mechanisms of telekin in human hepatocellular carcinoma HepG2 cells in vitro.
Methods: HepG2 cells were treated with telekin. Cell viability was evaluated using MTT assay. Flow cytometry was used to measure cell cycle profiles, ROS level and apoptosis. The protein expression levels were analyzed with Western blotting.

Results: Telekin (3.75–30 µmol/L) dose-dependently inhibited the viability of HepG2 cells and induced l apoptosis. Furthermore, the treatment induced cell cycle arrest at G2/M phase, accompanied by significantly increased the phosphorylation of Cdc25A and Cdc2, and decreased Cyclin B1 level. Moreover, the treatment significantly stimulated ROS production, and increased the phosphorylation of p38 and MAPKAPK-2 in the cells. Pretreatment with the antioxidant NAC (2.5, 5, and 10 mmol/L), or the p38 MAPK inhibitor SB203580 (2.5 and 5 µmol/L) dose-dependently attenuated these telekin-induced effects in the cells.

Conclusion: Telekin suppresses hepatocellular carcinoma cells in vitro by inducing G2/M phase arrest via activating the p38 MAPK pathway.

Keywords: Telekin; hepatocellular carcinoma; HepG2 cell; cell cycle arrest; ROS; p38 MAPK pathway; apoptosis; antioxidant; NAC; SB203580

This work was supported by grants from the National Natural Science Foundation of China (No 81273532).
# These authors contributed equally to this work.
* To whom correspondence should be addressed.
E-mail xiali@sdu.edu.cn
Received 2014-04-03 Accepted 2014-07-13

Article Options

Download Citation

Cited times in Scopus