## Abstract Notch signaling is involved in a variety of cellular processes, such as cell fate specification, differentiation, proliferation, and survival. Notch‐1 over‐expression has been reported in prostate cancer metastases. Likewise, Notch ligand Jagged‐1 was found to be over‐expressed in metas
Dauricine induces apoptosis, inhibits proliferation and invasion through inhibiting NF-κB signaling pathway in colon cancer cells
✍ Scribed by Zhengfeng Yang; Chenghai Li; Xiu Wang; Chunyan Zhai; Zhengfang Yi; Lei Wang; Bisheng Liu; Bing Du; Huihui Wu; Xizhi Guo; Mingyao Liu; Dali Li; Jian Luo
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 729 KB
- Volume
- 225
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
Abstract
Dauricine, a bioactive component of Asiatic Moonseed Rhizome, has been widely used to treat a large number of inflammatory diseases in traditional Chinese medicine. In our study, we demonstrated that dauricine inhibited colon cancer cell proliferation and invasion, and induced apoptosis by suppressing nuclear factor‐kappaB (NF‐κB) activation in a dose‐ and time‐dependent manner. Addition of dauricine inhibited the phosphorylation and degradation of IκBα, and the phosphorylation and translocation of p65. Moreover, dauricine down‐regulated the expression of various NF‐κB‐regulated genes, including genes involved cell proliferation (cyclinD1, COX2, and c‐Myc), anti‐apoptosis (survivin, Bcl‐2, XIAP, and IAP1), invasion (MMP‐9 and ICAM‐1), and angiogenesis (VEGF). In athymic nu/nu mouse model, we further demonstrated that dauricine significantly suppressed colonic tumor growth. Taken together, our results demonstrated that dauricine inhibited colon cancer cell proliferation, invasion, and induced cell apoptosis by suppressing NF‐κB activity and the expression profile of its downstream genes. These findings provide evidence for a novel role of dauricine in preventing or treating colon cancer through modulation of NF‐κB singling pathway. J. Cell. Physiol. 225: 266–275, 2010. © 2010 Wiley‐Liss, Inc.
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