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RETRACTED: FV‐429 Induced Apoptosis Through ROS‐Mediated ERK2 Nuclear Translocation and p53 Activation in Gastric Cancer Cells
Author(s) -
Zhou Yuxin,
Wei Libin,
Zhang Haiwei,
Dai Qinsheng,
Li Zhiyu,
Yu Boyang,
Guo Qinglong,
Lu Na
Publication year - 2015
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.25118
Subject(s) - apoptosis , kinase , p38 mitogen activated protein kinases , microbiology and biotechnology , cancer cell , chemistry , protein kinase a , chromosomal translocation , mtt assay , cancer research , biology , cancer , biochemistry , gene , genetics
Following our previous finding which revealed that FV‐429 induces apoptosis in human hepatocellular carcinoma HepG2 cells, in this study, we found that FV‐429 could also induce apoptosis in human gastric cancer cells. Firstly, FV‐429 inhibited the viability of BGC‐823 and MGC‐803 cells with IC 50 values in the range of 38.10 ± 6.28 and 31.53 ± 6.84 µM for 24 h treatment by MTT‐assay. Secondly, FV‐429 induced apoptosis in BGC‐823 and MGC‐803 cells through the mitochondrial‐mediated pathway, showing an increase in Bax/Bcl‐2 ratios, and caspase‐9 activation, without change in caspase‐8. Further research revealed that the mitogen‐activated protein kinases, including c‐Jun N‐terminal kinase, extracellular regulated kinase, and p38 mitogen‐activated protein kinase, could be activated by FV‐429‐induced high level ROS. Moreover, FV‐429 also promoted the ERK2 nuclear translocation, resulting in the co‐translocation of p53 to the nucleus and increased transcription of p53‐regulated proapoptotic genes. FV‐429 significantly inhibited the nude mice xenograft tumors growth of BGC‐823 or MGC‐803 cells in vivo. J. Cell. Biochem. 116: 1624–1637, 2015. © 2015 Wiley Periodicals, Inc.