Jellyfish extract induces apoptotic cell death through the p38 pathway and cell cycle arrest in chronic myelogenous leukemia K562 cells

PeerJ

Jong-Keun Son¹  Fansi Jin¹  Hyeun Wook Chang¹  Nam Gyu Park²  Young-Choon Lee³  Tae-Wook Chung⁴  Ki-Tae Ha⁴  Sun-Hyung Ha⁵  Choong-Hwan Kwak⁵  Jun-Young Park⁵  Cheorl-Ho Kim⁵  Fukushi Abekura⁵  Young-Chae Chang⁶ 

[1] College of Pharmacy, Yeungnam University, Gyeongsan, Gyeongsang, Republic of Korea;Department of Biotechnology, College of Fisheries Sciences, Pukyung National University, Busan, Republic of Korea;Department of Medicinal Biotechnology, College of Health Science, Dong-A University, Busan, Republic of Korea;Division of Applied Medicine, School of Korean Medicine, Pusan National University, Yangsan City, Gyeongsangnam-Do, Republic of Korea;Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Suwon City, Kyunggi-Do, Republic of Korea;Research Institute of Biomedical Engineering and Department of Medicine, Catholic University of Daegu, Daegu, Republic of Korea;

关键词: Jellyfish;    Jellyfish species;    Myelogenousleukemia k562 cells;   

DOI  :  10.7717/peerj.2895

来源: DOAJ

【 摘 要 】

Jellyfish species are widely distributed in the world’s oceans, and their population is rapidly increasing. Jellyfish extracts have several biological functions, such as cytotoxic, anti-microbial, and antioxidant activities in cells and organisms. However, the anti-cancer effect of Jellyfish extract has not yet been examined. We used chronic myelogenous leukemia K562 cells to evaluate the mechanisms of anti-cancer activity of hexane extracts from Nomura’s jellyfish in vitro. In this study, jellyfish are subjected to hexane extraction, and the extract is shown to have an anticancer effect on chronic myelogenous leukemia K562 cells. Interestingly, the present results show that jellyfish hexane extract (Jellyfish-HE) induces apoptosis in a dose- and time-dependent manner. To identify the mechanism(s) underlying Jellyfish-HE-induced apoptosis in K562 cells, we examined the effects of Jellyfish-HE on activation of caspase and mitogen-activated protein kinases (MAPKs), which are responsible for cell cycle progression. Induction of apoptosis by Jellyfish-HE occurred through the activation of caspases-3,-8 and -9 and phosphorylation of p38. Jellyfish-HE-induced apoptosis was blocked by a caspase inhibitor, Z-VAD. Moreover, during apoptosis in K562 cells, p38 MAPK was inhibited by pretreatment with SB203580, an inhibitor of p38. SB203580 blocked jellyfish-HE-induced apoptosis. Additionally, Jellyfish-HE markedly arrests the cell cycle in the G0/G1 phase. Therefore, taken together, the results imply that the anti-cancer activity of Jellyfish-HE may be mediated apoptosis by induction of caspases and activation of MAPK, especially phosphorylation of p38, and cell cycle arrest at the Go/G1 phase in K562 cells.

【 授权许可】

Unknown