Withaferin-A Inhibits Colon Cancer Cell Growth by Blocking STAT3 Transcriptional Activity.
10.15430/JCP.2015.20.3.185
- Author:
Bu Young CHOI
1
;
Bong Woo KIM
Author Information
1. Department of Pharmaceutical Science and Engineering, Seowon University, Cheongju, Korea.
- Publication Type:Original Article
- Keywords:
Withaferin-A;
Colorectal neoplasms;
STAT3 transcription factor;
Heterografts
- MeSH:
Animals;
Breast Neoplasms;
Colon*;
Colonic Neoplasms*;
Colorectal Neoplasms;
HCT116 Cells;
Heterografts;
Humans;
India;
Leukemia;
Mice;
Mice, Nude;
Plants, Medicinal;
STAT3 Transcription Factor;
Withania
- From:Journal of Cancer Prevention
2015;20(3):185-192
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Withania somnifera (known as Ashwagandha) is a medicinal plant used in the ayurvedic medicines in India. Withaferin-A, a withanolide derived from the leaf extract of W. somnifera, has been reported to exhibit anti-tumor activity against various cancer cells, such as leukemia, breast cancer and colon cancer cells. METHODS: We investigated the anti-cancer effects of withaferin-A on the proliferation and migration of human colorectal cancer (HCT116) cells. And we evaluated the effects of withaferin-A on the transcriptional activity of STAT3 and the growth of HCT116 cells in xenograft mouse tumor model. RESULTS: In the present study, we found that withaferin-A inhibited the proliferation and migration of HCT116 cells in a concentration-dependent manner. Treatment of HCT116 cells with withaferin-A attenuated interleukin-6-induced activation of STAT3, which has been implicated in the development and progression of colon cancer. To examine the effect of withaferin-A on HCT116 cells proliferation in vivo, we generated HCT116 cells xenograft tumors in Balb/c nude mice and treated the tumor bearing mice with or without withaferin-A intraperitoneally. Treatment with withaferin-A exhibited significant decrease in the volume and weight of tumors as compared to untreated controls. CONCLUSIONS: The present study suggests that withaferin-A holds the potential to be developed as a small molecule inhibitor of STAT3 for the treatment of HCT116.
