Atractylodin induces apoptosis through downregulation of PI3Kγ-mediated PI3K/Akt/mTOR/p70S6K signalling in colon cancer cells and suppresses the tumour formation in xenograft mice model

Abstract This study used both in vitro and in vivo models to evaluate the efficacy of atractylodin as an anticancer treatment for colorectal cancer. The cytotoxicity of atractylodin on colon cancer cells was assessed using the MTT assay, and atractylodin-induced apoptosis was determined using flow cytometry. The expression of cleaved caspase 3 and other apoptotic proteins was examined using Western blotting to determine the mechanism underlying atractylodin's anticancer activity. In addition, the role of PI3K/Akt/mTOR/p70S6K signalling in atractylodin-induced apoptosis in colon cancer cells was analyzed. The study found that atractylodin caused dose-dependent ROS-mediated apoptosis and DNA damage in colon cancer cells and activated caspase 3. Furthermore, atractylodin inhibited the PI3K/Akt/mTOR/p70S6K signalling pathway by targeting PI3Kγ in colon cancer cells. Molecular docking analysis indicated that atractylodin binds to the Akt binding pocket of PI3Kγ. The study also evaluated the antitumour effects of atractylodin on a colon cancer tumour xenograft model and found that it significantly reduced tumour growth and volume by inducing apoptosis. These results suggest that atractylodin has potential as a candidate for the treatment of colorectal cancer, although further research is necessary. Graphical abstract Atractylodin induces apoptosis in colon cancer cells.