BACKGROUND: Enterodiol (END) is transformed by human intestinal bacteria from lignans contained in various whole-grain cereals, nuts, legumes, flaxseed, and vegetables. It is known to have several physiological effects, but its effects on mitogen-activated protein kinase (MAPK) signaling and apoptosis in colorectal cancer (CRC) cells have not yet been elucidated. We therefore investigated the effects of END on apoptosis in CRC cells and whether these effects are mediated via MAPK signaling. RESULTS: Cell proliferation was decreased by END treatment in a time-dependent manner. In particular, END treatment resulted in an apoptosis rate of up to 40% in CT26 cells but showed no cytotoxicity toward RAW264.7 macrophages. Treatment with END also suppressed the migration of CRC cells in a concentration-dependent manner. The phosphorylation of extracellular signal-regulated kinase (ERK), jun N-terminal kinase (JNK), and p38 was down-regulated with END treatment. Furthermore, END decreased the expression levels of anti-apoptotic proteins in CRC cells. CONCLUSION: Enterodiol inhibited the growth of CRC cells by controlling the MAPK signaling pathway involved in proliferation and apoptosis. These results demonstrate that END has an apoptotic effect in CRC cells.
BACKGROUND:Enterodiol (END) is transformed by human intestinal bacteria from lignans contained in various whole-grain cereals, nuts, legumes, flaxseed, and vegetables. It is known to have several physiological effects, but its effects on mitogen-activated protein kinase (MAPK) signaling and apoptosis in colorectal cancer (CRC) cells have not yet been elucidated. We therefore investigated the effects of END on apoptosis in CRC cells and whether these effects are mediated via MAPK signaling. RESULTS: Cell proliferation was decreased by END treatment in a time-dependent manner. In particular, END treatment resulted in an apoptosis rate of up to 40% in CT26 cells but showed no cytotoxicity toward RAW264.7 macrophages. Treatment with END also suppressed the migration of CRC cells in a concentration-dependent manner. The phosphorylation of extracellular signal-regulated kinase (ERK), jun N-terminal kinase (JNK), and p38 was down-regulated with END treatment. Furthermore, END decreased the expression levels of anti-apoptotic proteins in CRC cells. CONCLUSION:Enterodiol inhibited the growth of CRC cells by controlling the MAPK signaling pathway involved in proliferation and apoptosis. These results demonstrate that END has an apoptotic effect in CRC cells.
Authors: Liliana Maribel Perez-Perez; José Ángel Huerta-Ocampo; Saúl Ruiz-Cruz; Francisco Javier Cinco-Moroyoqui; Francisco Javier Wong-Corral; Luisa Alondra Rascón-Valenzuela; Miguel Angel Robles-García; Ricardo Iván González-Vega; Ema Carina Rosas-Burgos; María Alba Guadalupe Corella-Madueño; Carmen Lizette Del-Toro-Sánchez Journal: Molecules Date: 2021-05-08 Impact factor: 4.411