Cancer Preventive Characteristics of Lignan Precursor vs. Lignan Metabolite in Human Colon Cancer SW480 Cells
Allan Ayella, Weiqun Wang
Abstract
Allan Ayella, Weiqun Wang
Abstract
Our previous studies demonstrated that lignan metabolites, enterolactone and enterodiol, inhibited colonic cancer cell growth by inducing cell cycle arrest and apoptosis. This study is focused on the cancer preventive impact of lignan secoisolariciresinol diglucoside (SDG), one of the prominent lignan glycoside, in human colonic cancer SW480 cells. Treatment with SDG at 0–40 μmol/L for 48 hrs resulted in a dose‐ and time‐dependent decrease in cell numbers, which was comparable to enterolactone. These cell growth inhibitions by SDG were not mediated by cytotoxicity, but rather linked to an increased cell cycle arrest at S‐phase. Furthermore, HPLC analysis indicated SDG in the media for 48 hrs was much more stable than enterolactone (stability at 95% for SDG in comparison to 57% for enterolactone). The intracellular levels of SDG rather than enterolactone were undetectable, suggesting that SDG was not readily absorbed or metabolized to its metabolites in this short‐term cell culture system. Taken together, these findings provide novel characteristics of dietary lignan precursor on colonic cancer growth inhibition and may enhance our understanding of bioavailability of dietary lignans for cancer prevention (supported by USDA Cooperative Project KS 680‐0199184).
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Our previous studies demonstrated that lignan metabolites, enterolactone and enterodiol, inhibited colonic cancer cell growth by inducing cell cycle arrest and apoptosis. This study is focused on the cancer preventive impact of lignan secoisolariciresinol diglucoside (SDG), one of the prominent lignan glycoside, in human colonic cancer SW480 cells. Treatment with SDG at 0–40 μmol/L for 48 hrs resulted in a dose‐ and time‐dependent decrease in cell numbers, which was comparable to enterolactone. These cell growth inhibitions by SDG were not mediated by cytotoxicity, but rather linked to an increased cell cycle arrest at S‐phase. Furthermore, HPLC analysis indicated SDG in the media for 48 hrs was much more stable than enterolactone (stability at 95% for SDG in comparison to 57% for enterolactone). The intracellular levels of SDG rather than enterolactone were undetectable, suggesting that SDG was not readily absorbed or metabolized to its metabolites in this short‐term cell culture system. Taken together, these findings provide novel characteristics of dietary lignan precursor on colonic cancer growth inhibition and may enhance our understanding of bioavailability of dietary lignans for cancer prevention (supported by USDA Cooperative Project KS 680‐0199184).
Key concepts: Enterolactone, Lignan, Chemistry, Metabolite, Cell growth, Cancer cell, Biochemistry, Cancer