Bornyl acetate extracted from Sharen () inhibits proliferation, invasion and induces apoptosis by suppressing phosphatidylinositol-3-kinase/protein kinase B signaling in colorectal cancer.

OBJECTIVE

To investigate the antitumor effects of bornyl acetate (BA) isolated from Sharen () in colorectal cancer (CRC) and the underlying mechanisms.

METHODS

SW480 and HT29 cells were treated with increasing doses of BA in order to determine its antitumor effects . Cell viability, colony formation, cell cycle, and apoptosis as well as migration and invasion were assessed using various assays. In addition, the antitumor effects of BA were assessed using a xenograft mouse model. We then assessed the mechanism of action of BA by conducting pathway activator-mediated rescue experiments and assessed the protein levels by Western blot analysis.

RESULTS

BA showed anti-CRC tumor activities by suppressing cell proliferation and colony formation, inducing apoptosis, blocking cell cycle, and inhibiting migration and invasion. These effects were mediated via suppression of the phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathway. In the tumor xenograft experiment, BA was found to repress tumor growth in vivo with low toxicity.

CONCLUSIONS

The results demonstrated that BA exerts antitumor effects by suppressing the PI3K/AKT pathway, with low toxicity. Thus, BA might be a potential novel therapeutic agent for CRC.