PURPOSE: Colon cancer is one of the deadly malignancies and the second most frequent cancer in the world. The development of drug resistance and dearth of the viable drug options forms an obstacle in the treatment of colon cancer. Herein, the anticancer potential of Apigenin was examined against cisplatin-resistant colon cancer cells. METHODS: The proliferation rate of the cisplatin-resistant colon cancer cell line HT-29 was assessed by WST-1 assay. Autophagy was detected by electron microscopy. Apoptotic cell death was analysed by propidium iodide (PI) staining. Cell cycle analysis was performed by flow cytometry. Protein expression was determined by immuno blotting. Xenografted mice models were used for in vivo evaluation of Apigenin. RESULTS: The results showed that Apigenin could considerably inhibit the proliferation of colon cancer cells. The anticancer activity of Apigenin against the HT-29 colon cancer cells was found to be due to induction of autophagy and apoptosis. The Apigenin-triggered apoptosis and autophagy were also linked with alteration in the apoptosis and autophagy-related protein expression. Furthermore, it was found that Apigenin could inhibit the m-TOR/PI3K/AKT signalling pathway in the cisplatin-resistant colon cancer cells. The effects of Apigenin were also examined in vivo in xenografted mice models and it was revealed that Apigenin inhibited the growth of xenografted tumors. CONCLUSIONS: Taken together, these results indicate that Apigenin could inhibit the growth of cisplatin-resistant colon cancer cells in vitro and in vivo and may be used for the improvement of therapy of colon cancer.
PURPOSE:Colon cancer is one of the deadly malignancies and the second most frequent cancer in the world. The development of drug resistance and dearth of the viable drug options forms an obstacle in the treatment of colon cancer. Herein, the anticancer potential of Apigenin was examined against cisplatin-resistant colon cancer cells. METHODS: The proliferation rate of the cisplatin-resistant colon cancer cell line HT-29 was assessed by WST-1 assay. Autophagy was detected by electron microscopy. Apoptotic cell death was analysed by propidium iodide (PI) staining. Cell cycle analysis was performed by flow cytometry. Protein expression was determined by immuno blotting. Xenografted mice models were used for in vivo evaluation of Apigenin. RESULTS: The results showed that Apigenin could considerably inhibit the proliferation of colon cancer cells. The anticancer activity of Apigenin against the HT-29 colon cancer cells was found to be due to induction of autophagy and apoptosis. The Apigenin-triggered apoptosis and autophagy were also linked with alteration in the apoptosis and autophagy-related protein expression. Furthermore, it was found that Apigenin could inhibit the m-TOR/PI3K/AKT signalling pathway in the cisplatin-resistant colon cancer cells. The effects of Apigenin were also examined in vivo in xenografted mice models and it was revealed that Apigenin inhibited the growth of xenografted tumors. CONCLUSIONS: Taken together, these results indicate that Apigenin could inhibit the growth of cisplatin-resistant colon cancer cells in vitro and in vivo and may be used for the improvement of therapy of colon cancer.
Authors: Monica Benvenuto; Loredana Albonici; Chiara Focaccetti; Sara Ciuffa; Sara Fazi; Loredana Cifaldi; Martino Tony Miele; Fernando De Maio; Ilaria Tresoldi; Vittorio Manzari; Andrea Modesti; Laura Masuelli; Roberto Bei Journal: Int J Mol Sci Date: 2020-09-10 Impact factor: 5.923