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Isoliquiritigenin inhibits migration and invasion of prostate cancer cells
Author(s) -
Kwon Gyoo Taik,
Cho Han J.,
Lim Soon Sung,
Shin HyunKyung,
Kim Eun Ji,
Chung WonYoon,
Park Jung Han Yoon
Publication year - 2006
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.20.4.a569-b
Subject(s) - du145 , chemistry , cell migration , isoliquiritigenin , cancer cell , matrix metalloproteinase , western blot , cancer research , tissue inhibitor of metalloproteinase , cancer , microbiology and biotechnology , cell , medicine , biology , biochemistry , lncap , gene
Isoliquiritigenin (ISL), 4,2′,4′‐trihydroxychalcone, found in licorice, shallot, and bean sprouts, is a potent antioxidant with anti‐inflammatory, anti‐platelet aggregation and anti‐carcinogenic effects. The purpose of the present study was to investigate the effects of ISL treatment on the migration and invasion characteristics of DU145 prostate cancer cells. DU145 cells were cultured in the presence of 0 – 20 μmol/L ISL with 10μng/mL EGF, 10 nmol/L IGF‐I, or 20 ng/mL heregulin‐β. EGF stimulated migration, whereas IGF‐I or hergulin had no effect. ISL inhibited the basal and EGF‐induced cell migration and invasion in dose‐dependent manners. Gelatin zymography and Western blot analysis exhibited a significant down‐regulation of matrix metalloproteinase (MMP)‐9 expression in DU145 cells stimulated with phorbol 12‐myristate 13‐aceate (PMA). ISL decreased the protein levels of tissue inhibitor of metalloproteinase‐1 (TIMP‐1) but increased TIMP‐2 levels in DU145 cells in a concentration‐dependent manner. In MatLyLu rat prostate cancer cells, ISL suppressed the protein levels of both pro and active MMP‐2 and ‐9 and mRNA levels of MMP‐2. These data therefore provide direct evidence for the role of ISL as a potent antimetastatic agent, which can markedly inhibit the metastatic and invasive capacity of malignant cells. The decrease in MMP‐9 and increase in TIMP‐2 expression may be one of mechanisms by which ISL inhibits cancer cell invasion.