Cytostatic inhibition of cancer cell growth by lignan secoisolariciresinol diglucoside

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dc.contributor.author Ayella, Allan
dc.contributor.author Lim, Soyoung
dc.contributor.author Jiang, Yu
dc.contributor.author Iwamoto, Takeo
dc.contributor.author Lin, Dingbo
dc.contributor.author Tomich, John M.
dc.contributor.author Wang, Weiqun
dc.date.accessioned 2010-12-10T21:04:01Z
dc.date.available 2010-12-10T21:04:01Z
dc.date.issued 2010-12-10
dc.identifier.uri http://hdl.handle.net/2097/6906
dc.description.abstract Our previous study demonstrated that lignan metabolites enterolactone and enterodiol inhibited colonic cancer cell growth by inducing cell cycle arrest and apoptosis. However, the dietary lignans are naturally present as glycoside precursors, such as secoisolariciresinol diglucoside (SDG), which have not been evaluated yet. This study tested the hypothesis that dietary SDG might have a different effect than its metabolites in human colonic SW480 cancer cells. Treatment with SDG at 0 to 40 μmol/L for up to 48 hours resulted in a dose- and time-dependent decrease in cell numbers, which was comparable to enterolactone. The inhibition of cell growth by SDG did not appear to be mediated by cytotoxicity, but by a cytostatic mechanism associated with an increase of cyclin A expression. Furthermore, high-performance liquid chromatography analysis indicated that SDG in the media was much more stable than enterolactone (95% of SDG survival vs 57% of enterolactone after 48-hour treatment). When the cells were treated with either enterolactone or SDG at 40 μmol/L for 48 hours, the intracellular levels of enterolactone, as measured by high-performance liquid chromatography–mass spectrometry/electron spray ionization, were about 8.3 × 10−8 nmol per cell; but intracellular SDG or potential metabolites were undetectable. Taken together, SDG demonstrated similar effects on cell growth, cytotoxicity, and cell cycle arrest when compared with its metabolite enterolactone. However, the reliable stability and undetectable intracellular SDG in treated cells may suggest that metabolism of SDG, if exposed directly to the colonic cells, could be different from the known degradation by microorganisms in human gut. en_US
dc.relation.uri http://www.elsevier.com/wps/find/journaldescription.cws_home/525483/ en_US
dc.subject Lignans en_US
dc.subject Secoisolariciresinol diglucoside en_US
dc.subject Enterolactone en_US
dc.subject Cancer prevention en_US
dc.subject SW480 cells en_US
dc.title Cytostatic inhibition of cancer cell growth by lignan secoisolariciresinol diglucoside en_US
dc.type Article (author version) en_US
dc.date.published 2010 en_US
dc.citation.doi doi:10.1016/j.nutres.2010.10.002 en_US
dc.citation.epage 769 en_US
dc.citation.issue 11 en_US
dc.citation.jtitle Nutrition Research en_US
dc.citation.spage 762 en_US
dc.citation.volume 30 en_US
dc.contributor.authoreid iwamoto en_US
dc.contributor.authoreid jtomich en_US
dc.contributor.authoreid wwang en_US


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