Vitexin-2-O-xyloside, raphasatin and (−)-epigallocatechin-3-gallate synergistically affect cell growth and apoptosis of colon cancer cells

• Published in: Food chemistry 2013-06, Vol.138 (2-3), p.1521-1530
• Main Authors: Papi, Alessio, Farabegoli, Fulvia, Iori, Renato, Orlandi, Marina, De Nicola, Gina R., Bagatta, Manuela, Angelino, Donato, Gennari, Lorenzo, Ninfali, Paolino
• Format: Article
• Language: English
• Subjects: (–)-Epigallocatechin-3-gallate; 4-Methylsulphanyl-3-butenyl isothiocyanate (raphasatin); Apigenin - pharmacology; apoptosis; Apoptosis - drug effects; Biological and medical sciences; breast neoplasms; breasts; Caspase 3 - metabolism; caspase-9; Catechin - analogs & derivatives; Catechin - pharmacology; cell growth; Cell Line, Tumor; Cell Proliferation - drug effects; Chemoprevention; colon; Colon carcinoma; Colonic Neoplasms - drug therapy; Colonic Neoplasms - physiopathology; colorectal neoplasms; cytotoxicity; Drug Synergism; Food industries; foods; Fundamental and applied biological sciences. Psychology; Humans; isothiocyanates; Isothiocyanates - pharmacology; lymphocytes; Mitochondria - drug effects; Mitochondria - metabolism; reactive oxygen species; Reactive Oxygen Species - metabolism; synergism; Vitexin-2-O-xyloside
• ISSN: 0308-8146; 1873-7072
• DOI: 10.1016/j.foodchem.2012.11.112

► Synergism of vitexin-2-O-xyloside, raphasatin and (−)-epigallocatechin-3-gallate. ► Treatments are cytotoxic to colon cancer cells but not to normal human lymphocytes. ► Treatments trigger ROS generation before apoptosis in colon cancer cells. Cytotoxic effects of the combination of the food components vitexin-2-O-xyloside (X), raphasatin (4-methylsulphanyl-3-butenyl isothiocyanates; G) and (–)-epigallocatechin-3-gallate (E) were investigated in colon (LoVo and CaCo-2) and breast (MDA-MB-231 and MCF-7) cancer cells. Breast cancer cells were more resistant than colon cells to X, G and E inhibition. On the contrary, marked synergistic effects among X, G and E on cell growth were found in both colon cancer cells. Further analysis revealed a G0/G1 arrest of the phase cell progression and apoptosis, linked to modulation of Bax, Bcl2, caspase-9 and poly(ADP-ribose) polymerase as well as Reactive Oxygen Species (ROS) generation in both colon cancer cells, whereas apoptosis and ROS were not significantly detected in normal human lymphocytes. We conclude that the X, G and E mixture might act by mitochondrial pathway activation of apoptosis, possibly elicited by ROS and the mixture may be effective in the chemoprevention of colon cancer.