PUBLICATION

Fucosterol Suppresses the Progression of Human Ovarian Cancer by Inducing Mitochondrial Dysfunction and Endoplasmic Reticulum Stress

Authors
Bae, H., Lee, J.Y., Song, G., Lim, W.
ID
ZDB-PUB-200521-2
Date
2020
Source
Marine drugs   18(5): (Journal)
Registered Authors
Keywords
ER, fucosterol, mitochondria, ovarian cancer, viability
MeSH Terms
  • Animals
  • Antineoplastic Agents/pharmacology*
  • Antineoplastic Agents/therapeutic use
  • Cell Line, Tumor/drug effects
  • Disease Models, Animal
  • Endoplasmic Reticulum Stress/drug effects*
  • Female
  • Humans
  • Mitochondria/drug effects*
  • Oceans and Seas
  • Ovarian Neoplasms/drug therapy
  • Phaeophyceae*
  • Stigmasterol/analogs & derivatives*
  • Stigmasterol/pharmacology
  • Stigmasterol/therapeutic use
  • Zebrafish
PubMed
32429354 Full text @ Mar. Drugs
Abstract
Ovarian cancer is difficult to diagnose early and has high rates of relapse and mortality. Therefore, the treatment of ovarian cancer needs to be improved. Recently, several studies have been conducted in an attempt to develop anticancer drugs from naturally derived ingredients. Compared to traditional chemotherapy, natural compounds can overcome drug resistance with lower side effects. Fucosterol, a phytosterol present in brown algae, reportedly possesses many bioactive effects, including anticancer properties. However, the anticancer effects of fucosterol in ovarian cancer remain unexplored. Therefore, we investigated the effects of fucosterol on progression in human ovarian cancer cells. Fucosterol inhibited cell proliferation and cell-cycle progression in ovarian cancer cells. Additionally, fucosterol regulated the proliferation-related signaling pathways, the production of reactive oxygen species, mitochondrial function, endoplasmic reticulum stress, angiogenesis, and calcium homeostasis. Moreover, it decreased tumor formation in a zebrafish xenograft model. These results indicate that fucosterol could be used as a potential therapeutic agent in ovarian cancer.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping