1. Asparanin A induces G2/M cell cycle arrest and apoptosis in human hepatocellular carcinoma HepG2 cells
- Author
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Wei Liu, Li Yang, Dandan Gong, Qinglong Guo, Qinsheng Dai, Qi Qi, Na Lu, Xue-Feng Huang, Ling-Yi Kong, and Fei-Fei Nie
- Subjects
Cyclin-Dependent Kinase Inhibitor p21 ,G2 Phase ,Carcinoma, Hepatocellular ,Cell cycle checkpoint ,Cell ,Cyclin A ,Biophysics ,Apoptosis ,Biochemistry ,Cell Line, Tumor ,CDC2 Protein Kinase ,medicine ,Humans ,Cytotoxic T cell ,Molecular Biology ,Cyclin-dependent kinase 1 ,biology ,Cell Cycle ,Cyclin-Dependent Kinase 2 ,Liver Neoplasms ,Cell Biology ,Saponins ,Cell cycle ,Antineoplastic Agents, Phytogenic ,Cell biology ,medicine.anatomical_structure ,Cell culture ,Cancer research ,biology.protein ,Asparagus Plant ,Cell Division - Abstract
We recently established that asparanin A, a steroidal saponin extracted from Asparagus officinalis L., is an active cytotoxic component. The molecular mechanisms by which asparanin A exerts its cytotoxic activity are currently unknown. In this study, we show that asparanin A induces G(2)/M phase arrest and apoptosis in human hepatocellular carcinoma HepG2 cells. Following treatment of HepG2 cells with asparanin A, cell cycle-related proteins such as cyclin A, Cdk1 and Cdk4 were down-regulated, while p21(WAF1/Cip1) and p-Cdk1 (Thr14/Tyr15) were up-regulated. Additionally, we observed poly (ADP-ribose) polymerase (PARP) cleavage and activation of caspase-3, caspase-8 and caspase-9. The expression ratio of Bax/Bcl-2 was increased in the treated cells, where Bax was also up-regulated. We also found that the expression of p53, a modulator of p21(WAF1/Cip1) and Bax, was not affected in asparanin A-treated cells. Collectively, our findings demonstrate that asparanin A induces cell cycle arrest and triggers apoptosis via a p53-independent manner in HepG2 cells. These data indicate that asparanin A shows promise as a preventive and/or therapeutic agent against human hepatoma.
- Published
- 2009