PURPOSE: To investigate the anticancer effects of Trifolirhizin in SNU-5 human gastric cancer cells along with evaluation of its effects on autophagy, apoptosis, cell cycle phase distribution and m-TOR/PI3K signalling pathway. METHODS: The antiproliferative effect on gastric cancer cells was assessed by MTT assay. Autophagy was detected by electron microscopy and western blot. Apoptotic cell death was revealed by acridine orange (AO)/ethidium bromide (EB) and annexin V/propidium iodide (PI) staining using flow cytometry. Cell cycle analysis was carried out by flow cytometry. Protein expression was determined by immunoblotting. Xenografted mice models were used to evaluate in vivo the anticancer effects of Trifolirhizin. RESULTS: Trifolirhizin could significantly inhibit the proliferation of the gastric cancer cells. The anticancer activity of Trifolirhizin against the gastric cancer cells was found to be due to induction of autophagy and mitochondrial-mediated apoptosis. It was further observed that both apoptosis and autophagy-related protein expressions sere significantly altered. Further, it was found that Trifolirhizin could inhibit the m-TOR/PI3K/AKT signalling pathway. In vivo evaluation in xenografted mice indicated that Trifolirhizin inhibited significantly both tumor weight and tumor volume. CONCLUSIONS: In conclusion, it can be safely stated that Trifolirhizin has the potential to be developed as a potent anticancer agent against gastric carcinoma provided further in depth evaluation of this compound is performed.
PURPOSE: To investigate the anticancer effects of Trifolirhizin in SNU-5 humangastric cancer cells along with evaluation of its effects on autophagy, apoptosis, cell cycle phase distribution and m-TOR/PI3K signalling pathway. METHODS: The antiproliferative effect on gastric cancer cells was assessed by MTT assay. Autophagy was detected by electron microscopy and western blot. Apoptotic cell death was revealed by acridine orange (AO)/ethidium bromide (EB) and annexin V/propidium iodide (PI) staining using flow cytometry. Cell cycle analysis was carried out by flow cytometry. Protein expression was determined by immunoblotting. Xenografted mice models were used to evaluate in vivo the anticancer effects of Trifolirhizin. RESULTS:Trifolirhizin could significantly inhibit the proliferation of the gastric cancer cells. The anticancer activity of Trifolirhizin against the gastric cancer cells was found to be due to induction of autophagy and mitochondrial-mediated apoptosis. It was further observed that both apoptosis and autophagy-related protein expressions sere significantly altered. Further, it was found that Trifolirhizin could inhibit the m-TOR/PI3K/AKT signalling pathway. In vivo evaluation in xenografted mice indicated that Trifolirhizin inhibited significantly both tumor weight and tumor volume. CONCLUSIONS: In conclusion, it can be safely stated that Trifolirhizin has the potential to be developed as a potent anticancer agent against gastric carcinoma provided further in depth evaluation of this compound is performed.