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Genistein represses invasion in an in vitro colon cancer metastasis model by transcriptionally upregulating metastasis repressor NDRG1
Author(s) -
Li Qian,
Chen Hong
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.116.6
Subject(s) - genistein , metastasis , cancer research , cancer , epigenetics , biology , cell culture , metastasis suppressor , colorectal cancer , metastasis suppressor gene , cell adhesion , cell , gene , endocrinology , genetics
Cancer metastasis accounts for most cancer deaths. Genistein, a biologically active soy isoflavone, has been indicated as an inhibitor of cancer progression. In this study, we tested our hypothesis that genistein can repress colon cancer metastasis in vitro by modifying the expression of metastasis suppressor NDRG1. Cell models SW480 and SW620 which are poorly and highly metastatic human colon cancer cell lines respectively, were used. Genistein treatment reduced the proliferation and wound healing ability of both cell lines. Interestingly, genistein specifically increased the adhesion of the metastatic cell line SW620 and inhibited the migration of SW620. Moreover, genistein increased the mRNA expression of NDRG1 in both cell lines. The low NDRG1 gene expression in SW620 compared to that in SW480 is associated with altered chromatin configuration of the gene. In conclusion, genistein treatment increased expression of several genes responsible for metastasis repression in SW620. Future research will focus on illustrating the epigenetic mechanisms underlining the metastasis inhibiting effects by genistein. Grant Funding Source : University of Illinois at Urbana‐Champaign