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Eupatilin Promotes Cell Death by Calcium Influx through ER-Mitochondria Axis with SERPINB11 Inhibition in Epithelial Ovarian Cancer

Authors
Lee, Jin-YoungBae, HyocheolYang, ChangwonPark, SunwooYoun, Byung-SooKim, Han-SooSong, GwonhwaLim, Whasun
Issue Date
6월-2020
Publisher
MDPI
Keywords
SERPINB11; ovarian cancer; eupatilin; calcium influx; ER-mitochondria axis
Citation
CANCERS, v.12, no.6
Indexed
SCIE
SCOPUS
Journal Title
CANCERS
Volume
12
Number
6
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/55466
DOI
10.3390/cancers12061459
ISSN
2072-6694
Abstract
Ovarian cancer is the leading cause of gynecological cancer-related mortality. The anticancer effect of eupatilin, a family of flavonoids, is known in many cancer types, but it is unclear what mechanism it plays in ovarian cancer. In this study, eupatilin promoted cell death of ovarian cancer cells by activating caspases, cell cycle arrest, reactive oxygen species (ROS) generation, calcium influx, disruption of the endoplasmic reticulum (ER)-mitochondria axis with SERPINB11 inhibition, and downregulation of phosphoinositide 3-kinase (PI3K) and mitogen activated protein kinase (MAPK) pathways. Additionally, eupatilin-reduced SERPINB11 expression enhanced the effect of conventional chemotherapeutic agents against ovarian cancer cell progression. Cotreatment with siSERPINB11 and eupatilin increased calcium-ion-dependent apoptotic activity in ovarian cancer cells. Although there were no significant toxic effects of eupatilin on embryos, eupatilin completely inhibited tumorigenesis in a zebrafish xenograft model. In addition, eupatilin suppressed angiogenesis in zebrafish transgenic models. Collectively, downregulating SERPINB11 with eupatilin against cancer progression may improve therapeutic activity.
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