Costunolide Induces Apoptosis through Generation of ROS and Activation of P53 in Human Esophageal Cancer Eca‐109 Cells. Issue 9 (14th April 2016)

• Record Type: Journal Article
• Authors: Hua, Peiyan; Sun, Mei; Zhang, Guangxin; Zhang, Yifan; Song, Ge; Liu, Zhenyu; Li, Xin; Zhang, Xingyi; Li, Bingjin
• Is Part Of: Journal of biochemical and molecular toxicology. Volume 30:Issue 9(2016:Sep.)
• Page Start: 462
• Page End: 469
• Publication Date: 2016-04-14
• Subjects: Sophageal Cancer -- Costunolide -- Apoptosis -- G1/S Phase -- ROS; Biochemistry -- Periodicals; Molecular biology -- Periodicals; Toxicology -- Periodicals; 574
• DOI: 10.1002/jbt.21810
• Languages: English
• ISSNs: 1095-6670

Abstract

ABSTRACT: Costunolide is a sesquiterpene lactone, which possesses potent anti‐cancer properties. However, there is little report about its effects on esophageal cancer. In our study, we investigated the effects of costunolide on the cell viability, cell cycle, and apoptosis in human esophageal cancer Eca‐109 cells. It was found that costunolide inhibited the growth of Eca‐109 cells in a dose‐dependent manner, which was associated with the loss of mitochondrial membrane potential (Δψm ) and the production of ROS. Costunolide induced apoptosis of Eca‐109 cells as well as cell cycle arrest in G1/S phase by upregulation of P53 and P21. Costunolide triggered apoptosis in esophageal cancer cells via the upregulation of Bax, downregulation of Bcl‐2, and significant activation of caspase‐3 and poly ADP‐ribose polymerase. These effects were markedly abrogated when cells were pretreated with N‐acetylcysteine, a specific reactive oxygen specie inhibitor. These results suggest that costunolide is a potential candidate for the treatment of esophageal cancer.