| Literature DB >> 22464014 |
Juanjuan Liu1, Min Shen, Zhenggang Yue, Zhifu Yang, Meng Wang, Chen Li, Chunyan Xin, Yukun Wang, Qibing Mei, Zhipeng Wang.
Abstract
Triptolide, a diterpene triepoxide compound extracted from the traditional Chinese medicine herb Tripterygium wilfordii Hook F., is a potential cancer chemotherapeutic for tumors. However, the mechanism of anti-proliferative mechanism of triptolide in colon cancer cells is not entirely clear. Triptolide markedly inhibited HT29 and SW480 cells proliferation in a dose- and time-dependent manner. Triptolide decreased ERK and AKT phosphorylation, and GABPα expression in colon cancer cells. Beta-catenin expression and phosphorylation were not altered by incubation of triptolide. However, we found that triptolide repressed expression of LEF/TCF. Although it did not significantly affect cells apoptosis, triptolide induced G1 phase arrest dose-dependently. Further detection for the expression of cell cycle-related proteins suggesting that triptolide stimulate expression of p21 and repress cyclin A1. Increased p21 binded to CDK4/CDK6, therefore blocked function of CDK4/CDK6, and subsequently contribute to the G1 arrest. These data suggested that triptolide is a potential agent for treatment of colon cancer, and its anti-proliferation effect mainly occur through G1 phase arrest.Entities:
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Year: 2012 PMID： 22464014 DOI： 10.1016/j.phymed.2012.02.014
Source DB: PubMed Journal: Phytomedicine ISSN： 0944-7113 Impact factor: 5.340