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Costunolide Induces Apoptosis through Generation of ROS and Activation of P53 in Human Esophageal Cancer Eca‐109 Cells
Author(s) -
Hua Peiyan,
Sun Mei,
Zhang Guangxin,
Zhang Yifan,
Song Ge,
Liu Zhenyu,
Li Xin,
Zhang Xingyi,
Li Bingjin
Publication year - 2016
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21810
Subject(s) - downregulation and upregulation , apoptosis , reactive oxygen species , cell cycle , cancer cell , viability assay , cancer research , cell cycle checkpoint , chemistry , cancer , biology , microbiology and biotechnology , biochemistry , gene , genetics
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 (Δψ m ) 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.