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

PeerJ

article

Sun-Hyung Ha¹  Fansi Jin²  Choong-Hwan Kwak¹  Fukushi Abekura¹  Jun-Young Park¹  Nam Gyu Park³  Young-Chae Chang⁴  Young-Choon Lee⁵  Tae-Wook Chung⁶  Ki-Tae Ha⁶  Jong-Keun Son²  Hyeun Wook Chang²  Cheorl-Ho Kim¹ 

[1] Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University;College of Pharmacy, Yeungnam University;Department of Biotechnology, College of Fisheries Sciences, Pukyung National University;Research Institute of Biomedical Engineering and Department of Medicine, Catholic University of Daegu;Department of Medicinal Biotechnology, College of Health Science, Dong-A University;Division of Applied Medicine, School of Korean Medicine, Pusan National University

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

DOI  :  10.7717/peerj.2895

学科分类：社会科学、人文和艺术（综合）

来源: Inra

【 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】

CC BY