Arglabin is a plant sesquiterpene lactone that exerts potent anticancer effects on human oral squamous cancer cells via mitochondrial apoptosis and downregulation of the mTOR/PI3K/Akt signaling pathway to inhibit tumor growth in vivo.

Purpose: To evaluate the anticancer effects and the underlying mechanism of arglabin on oral squamous cell carcinoma (OSCC) cells. Methods: 4',6-Diamidino-2-phenylindole dihydrochloride (DAPI) and annexin V/propidium iodide (PI) staining were performed to evaluate apoptosis. Reactive oxygen species (ROS) levels and mitochondrial membrane potential (MMP) were examined by flow cytometry. Protein expression was assessed by western blot analysis. To examine the anticancer activity of arglabin in vivo, subcutaneous xenografts in nude mice were evaluated. Results: Arglabin exhibited an IC50 of 10 mu m in OSCC cells and induced apoptosis by inhibiting MMP and enhancing intracellular ROS levels. DAPI and annexin V/PI staining indicated apoptosis of OSCC cells induced by arglabin. Arglabin also downregulated the expression of key proteins in the mTOR/PI3K/Akt signaling pathway. In vivo evaluation showed that arglabin reduced the average tumor volumes and growth of xenografted tumors, indicative of its anticancer activity. Conclusions: Arglabin showed selective in vitro and in vivo anticancer activities against OSCC cells and is therefore a potential therapeutic agent for the management of OSCC.