TY - JOUR
T1 - Myricetin inhibits endometriosis growth through cyclin E1 down-regulation in vitro and in vivo
AU - Park, Sunwoo
AU - Song, Gwonhwa
AU - Lim, Whasun
N1 - Funding Information:
This research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute funded by the Ministry of Health & Welfare (grant no. HI17C0929) and the National Research Foundation of Korea(NRF) grant funded by the Ministry of Science and ICT (no. 2018R1C1B6009048). The authors declare that there are no conflicts of interest.
Funding Information:
This research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute funded by the Ministry of Health & Welfare (grant no. HI17C0929 ) and the National Research Foundation of Korea(NRF) grant funded by the Ministry of Science and ICT (no. 2018R1C1B6009048 ).
Publisher Copyright:
© 2020 Elsevier Inc.
PY - 2020/4
Y1 - 2020/4
N2 - 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.
AB - 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.
KW - Antiproliferation
KW - CCNE1
KW - Cell cycle
KW - Endometriosis
KW - Myricetin
UR - http://www.scopus.com/inward/record.url?scp=85077924918&partnerID=8YFLogxK
U2 - 10.1016/j.jnutbio.2019.108328
DO - 10.1016/j.jnutbio.2019.108328
M3 - Article
C2 - 31952013
AN - SCOPUS:85077924918
SN - 0955-2863
VL - 78
JO - Journal of Nutritional Biochemistry
JF - Journal of Nutritional Biochemistry
M1 - 108328
ER -
