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Anti‐proliferative effects of physiological concentrations of enterolactone in models of prostate tumourigenesis
Author(s) -
McCann Mark J.,
Rowland Ian R.,
Roy Nicole C.
Publication year - 2013
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201200362
Subject(s) - lncap , enterolactone , cell growth , biology , prostate , cell culture , cell cycle , prostate cancer , cancer research , microbiology and biotechnology , cell , chemistry , endocrinology , genetics , cancer , phytoestrogens , estrogen
Scope There is evidence that a mammalian lignan, enterolactone ( ENL ), decreases the proliferation rate of prostate cancer cells, although previous studies have used concentrations difficult to achieve through dietary modification. We have therefore investigated the anti‐proliferative effects of ENL in an in vitro model of prostate tumourigenesis at concentrations reported to occur in a range of male populations. Methods and results The effects of 0.1 and 1 μM ENL on three markers of viability and proliferation (metabolic activity, growth kinetics, and cell cycle progression) were assessed in the RWPE ‐1, WPE 1‐ NA 22, WPE 1‐ NB 14, WPE 1‐ NB 11, WPE 1‐ NB 26, LNC a P , and PC ‐3 cell lines over 72 h. Based on these data, we quantified the expression levels of 12 genes involved in the control of DNA replication initiation using T aq M an real‐time PCR in the WPE 1‐ NA 22, WPE 1‐ NB 14, WPE 1‐ NB 11, and WPE 1‐ NB 26 cell lines. ENL significantly inhibited the abnormal proliferation of the WPE 1‐ NB 14 and WPE 1‐ NB 11 cell lines and appears to be a consequence of decreased expression of abnormal chromatin licensing and DNA replication factor 1. Conclusion In contrast to previous studies, concentrations of ENL that are reported after dietary intervention restrict the proliferation of early‐stage tumourigenic prostate cell lines by inhibiting the abnormal formation of complexes that initiate DNA replication.