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Eupatilin Promotes Cell Death by Calcium Influx through ER-Mitochondria Axis with SERPINB11 Inhibition in Epithelial Ovarian Cancer.
- Source :
- Cancers; Jun2020, Vol. 12 Issue 6, p1459, 1p
- Publication Year :
- 2020
-
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. [ABSTRACT FROM AUTHOR]
- Subjects :
- CALCIUM metabolism
REACTIVE oxygen species
ANIMAL experimentation
ANTINEOPLASTIC agents
APOPTOSIS
BIOCHEMISTRY
ENDOPLASMIC reticulum
FISHES
GENE expression
PHENOMENOLOGY
MITOCHONDRIA
PHOSPHOTRANSFERASES
SERINE
EMBRYOS
PROTEASE inhibitors
MITOGEN-activated protein kinases
TREATMENT effectiveness
CASPASES
FLAVONES
CANCER cell culture
OVARIAN epithelial cancer
CHEMICAL inhibitors
PHARMACODYNAMICS
Subjects
Details
- Language :
- English
- ISSN :
- 20726694
- Volume :
- 12
- Issue :
- 6
- Database :
- Complementary Index
- Journal :
- Cancers
- Publication Type :
- Academic Journal
- Accession number :
- 144495701
- Full Text :
- https://doi.org/10.3390/cancers12061459