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Myricetin inhibits endometriosis growth through cyclin E1 down-regulation in vitro and in vivo

Authors
Park, SunwooSong, GwonhwaLim, Whasun
Issue Date
4월-2020
Publisher
ELSEVIER SCIENCE INC
Keywords
Myricetin; Endometriosis; Antiproliferation; CCNE1; Cell cycle
Citation
JOURNAL OF NUTRITIONAL BIOCHEMISTRY, v.78
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Volume
78
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/56707
DOI
10.1016/j.jnutbio.2019.108328
ISSN
0955-2863
Abstract
Endometriosis is a benign gynecological condition prevalent among reproductive-aged women. Although active research and studies have been carried out to discover new drugs, surgery and hormone therapy are still the gold standard for endometriosis treatment. Nowadays, various flavonoids are considered long-term supplements for different diseases. Myricetin, a flavonol, has antiproliferative, anti- or pro-oxidant, and anticancer effects in gynecological diseases. Here, we reveal for the first time, to our knowledge, the antigrowth effects of myricetin in endometriosis. Myricetin inhibited cell proliferation and cell cycle progression of human VK2/E6E7 and End1/E6E7 cells and induced apoptosis, with the loss of mitochondrial membrane potential and accumulation of reactive oxygen species and calcium ions. Additionally, myricetin decreased the activation of AKT and ERK1/2 proteins, whereas it induced p38 activation in both cell lines. Moreover, myricetin decreased lesion size in the endometriosis mouse model via Ccne1 inhibition. Thus, myricetin has antiproliferative effects on endometriosis through cell cycle regulation. (C) 2019 Elsevier Inc. All rights reserved.
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융합생명공학과
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