Recent research suggests a relationship between
cancer progression and oxidative mechanisms. Among the phenolic compounds such as
tracheloside (TCS) are a major bioactive compound that can combat
oxidant stress-related
chronic diseases and that also displays anti-
tumor activity. Although TCS can inhibit mammalian
carcinoma, its effects on
colorectal cancer (CRC) have not been clarified. The purpose of this study was to investigate the effects of TCS on the proliferation of CRC cells, the
metastasis of CT26 cells, and the molecular mechanisms related to TCS in vitro and in vivo. A cell viability assay showed that TCS inhibited the proliferation of CRC cells. TCS-treated CT26 cells were associated with the upregulation of p16 as well as the downregulation of
cyclin D1 and CDK4 in cell cycle arrest. In addition, TCS induced apoptosis of CT26 cells through mitochondria-mediated apoptosis and regulation of the Bcl-2 family. Expression of epithelial-mesenchymal transition (EMT) markers was regulated by TCS treatment in CT26 cells. TCS significantly inhibited the lung
metastasis of CT26 cells in a mouse model. These results suggest that TCS, by inducing cell cycle arrest and apoptosis through its
anti-oxidant properties, is a novel therapeutic agent that inhibits metastatic phenotypes of murine CRC cells.