Growth inhibition and induction of apoptosis in human oral squamous cell carcinoma Tca-8113 cell lines by shikonin was partly through the inactivation of NF-κB pathway
Article first published online: 31 DEC 2007
Copyright © 2007 John Wiley & Sons, Ltd.
Volume 22, Issue 3, pages 407–415, March 2008
How to Cite
Ruan, M., Ji, T., Yang, W., Duan, W., Zhou, X., He, J., Zhou, J., Chen, W. and Zhang, C. (2008), Growth inhibition and induction of apoptosis in human oral squamous cell carcinoma Tca-8113 cell lines by shikonin was partly through the inactivation of NF-κB pathway. Phytother. Res., 22: 407–415. doi: 10.1002/ptr.2340
- Issue published online: 28 FEB 2008
- Article first published online: 31 DEC 2007
- Manuscript Revised: 31 JUL 2007
- Manuscript Accepted: 31 JUL 2007
- Manuscript Received: 29 JAN 2007
- National Natural Science Fund of China. Grant Number: 30300389
- oral squamous cell carcinoma (OSCC);
- growth inhibition;
- caspase family
Shikonin, a naphthoquinone pigment isolated from the Chinese herbal therapeutic, Zicao, has been shown to exhibit antioxidant and anticancer effects. In this study, its ability to induce apoptosis in cultured Tca-8113 oral cancer cells was studied. Treatment of the Tca-8113 cells with a variety of concentrations of Shikonin (10–40 µm) resulted in dose- and time-dependent sequences of events marked by apoptosis, as shown by the loss of cell viability, chromatin condensation, internucleosomal DNA fragmentation and sub-G1 phase accumulation. Furthermore, apoptosis in the Tca-8113 cells was accompanied by the activation of protease caspase-8, -9, -3 and low expression of Bcl-2 protein. Interestingly, inactivation of the NF-κB pathway was found in shikonin-induced apoptosis in Tca-8113 cells. These results raise the possibility that the anti-tumor effects of Shikonin in Tca-8113 cells are at least partly through the inactivation of the NF-κB pathway and subsequent activation of protease caspase family. Pharmacological inhibition of the NF-κB activity by Shikonin might be a powerful treatment option for OSCC in which activation of NF-κB plays a critical role in tumor growth and progression. Copyright © 2007 John Wiley & Sons, Ltd.