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The Inhibitory Effect of Roasted Licorice Extract on Human Metastatic Breast Cancer Cell‐Induced Bone Destruction
Author(s) -
Lee Sun Kyoung,
Park KwangKyun,
Park Jung Han Yoon,
Lim Soon Sung,
Chung WonYoon
Publication year - 2013
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.4930
Subject(s) - inhibitory postsynaptic potential , traditional medicine , medicine , breast cancer , metastatic breast cancer , pharmacology , mcf 7 , glycyrrhiza , pharmacognosy , cancer , chemistry , human breast , biological activity , in vitro , pathology , biochemistry , alternative medicine
The aim of this study was to determine whether the ethanol extract of roasted licorice (rLE) could inhibit breast cancer‐mediated bone destruction. rLE treatment reduced the viability of MDA‐MB‐231 human metastatic breast cancer cells but did not show any cytotoxicity in hFOB1.19 human osteoblastic cells and murine bone marrow‐derived macrophages (BMMs). rLE inhibited expression and secretion of receptor activator of nuclear factor κB ligand (RANKL) as well as the mRNA and protein expression of cyclooxygenase‐2 in osteoblastic cells exposed to the conditioned medium of breast cancer cells. rLE dramatically inhibited RANKL‐induced osteoclastogenesis in BMMs, thereby reducing osteoclast‐mediated pit formation. Moreover, treatment with licochalcone A and isoliquiritigenin as the active components, whose contents are increased by the roasting process, remarkably suppressed RANKL‐induced osteoclast formation in BMMs, respectively. Furthermore, orally administered rLE substantially blocked tumor growth and bone destruction in mice inoculated with breast cancer cells in the tibiae. Serum levels of tartrate‐resistant acid phosphatase and C‐terminal cross‐linking telopeptide of type I collagen and trabecular bone morphometric parameters were reversed to almost the same levels as the control mice by the rLE treatment. In conclusion, rLE may be a beneficial agent for preventing and treating bone destruction in patients with breast cancer. Copyright © 2013 John Wiley & Sons, Ltd.