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The effects of talosin A on the proliferation of breast cancer cells and RANKL‐OPG expression in osteoblasts
Author(s) -
Kang SeChan,
Kang NamSung,
Pyo Suhkneung,
Sohn EunHwa
Publication year - 2010
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.24.1_supplement.928.26
Subject(s) - rankl , osteoprotegerin , chemistry , osteoblast , endocrinology , medicine , cell growth , activator (genetics) , receptor , microbiology and biotechnology , cancer research , biology , biochemistry , in vitro
Talosin A from Kitasatospora kifunensis MJM341 is a novel isoflavonol glycoside with 6‐deoxy‐L‐talose at C‐4 of L‐rhamnose as a sugar moiety. In this study, we investigated the effect of talosin A on the proliferation of MCF7‐BUS, breast cancer cells (ER+). Tamoxifen, ER antagonist, inhibited the cell proliferation which was significantly increased by talosin A (1, 10 and 100μM) in MCF7‐BUS cells. In addition, ER‐reporter analysis showed that talosin A increased the binding activity of ERα. RANKL (receptor activator of nuclear factor κ‐B) and osteoprotegerin (OPG), which are both produced by osteoblasts at different stages of maturity. To investigate the effect of talosin A on the differentiation of osteoblasts, we examined the expression of RANKL and OPG by RT‐PCR assay in MG‐63, osteoblast‐like cells. The treatment of talosin A down‐regulated RANKL/OPG ratio, which means inhibitory regulation of osteocalsts activation. These data suggest that talosin A might affect the role of osteoblasts like bone formation and might increase ER+ cell proliferation via binding of ERα.