Methyl linderone suppresses TPA-stimulated IL-8 and MMP-9 expression via the ERK/STAT3 pathway in MCF-7 breast cancer cells

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Title
Methyl linderone suppresses TPA-stimulated IL-8 and MMP-9 expression via the ERK/STAT3 pathway in MCF-7 breast cancer cells
Author(s)
J H Yoon; T H Pham; J Lee; J Lee; Hyung Won RyuSei-Ryang Oh; J W Oh; D Y Yoon
Bibliographic Citation
Journal of Microbiology and Biotechnology, vol. 30, no. 3, pp. 325-332
Publication Year
2020
Abstract
Methyl linderone (ML), a cyclo-pentenedione, was isolated from the fruit of Lindera erythrocarpa Makino (family Lauraceae). This plant has well-known anti-inflammatory effects; however, the anti-cancer effects of ML have not yet been reported. Thus, in the present study we investigated the effects of ML on the metastasis of human breast cancer cells. We used 12-O-tetradecanoyl phorbol-13-acetate (TPA)-stimulated MCF-7 cells as the cell model to study the effects of ML on invasion and migration. ML was found to reduce the invasion and migration rate of TPA-stimulated MCF-7 cells. Moreover, it inhibited two metastasis-related factors, matrix metalloproteinase-9 (MMP-9) and interleukin-8 (IL-8), at the mRNA and protein expression levels, in TPA-treated MCF-7 cells. The mechanism by which ML exerted these effects was through the inhibition of translocation of activator protein-1 (AP-1) and signal transducer and activator of transcription-3 (STAT3), mediated via phosphorylation of extracellular signal-regulated kinase (ERK). Taken together, our findings indicated that ML attenuated the TPA-stimulated invasion and migration of MCF-7 cells by suppressing the phosphorylation of ERK and its downstream factors, AP-1 and STAT3. Therefore, ML is a potential agent for the treatment of breast cancer metastasis.
Keyword
IL-8MCF-7 cellsMMP-9Methyl linderonemetastasis
ISSN
1017-7825
Publisher
Korea Soc-Assoc-Inst
DOI
http://dx.doi.org/10.4014/jmb.1911.11068
Type
Article
Appears in Collections:
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
Ochang Branch Institute > 1. Journal Articles
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