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Apoptotic effect of enterodiol, the final metabolite of edible lignans, in colorectal cancer cells
Author(s) -
Shin MinKyoung,
Jeon YongDeok,
Jin JongSik
Publication year - 2018
Publication title -
journal of the science of food and agriculture
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 142
eISSN - 1097-0010
pISSN - 0022-5142
DOI - 10.1002/jsfa.9448
Subject(s) - apoptosis , mapk/erk pathway , kinase , p38 mitogen activated protein kinases , signal transduction , cancer research , protein kinase a , colorectal cancer , cell growth , microbiology and biotechnology , mitogen activated protein kinase , biology , chemistry , cancer , biochemistry , genetics
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. © 2018 Society of Chemical Industry