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Journal of Cancer Prevention

Original Article

Cancer prevention research 2011; 16(2): 126-133

Published online June 30, 2011

© Korean Society of Cancer Prevention

Induction of Apoptosis by J-7, a Methyl Jasmonate Derivative, in Human Hepatocarcinoma Hep3B Cells through Activation of the ERK and JNK

Cheol Park and Yung Hyun Choi


In the present study, it was investigated that the effects of mitogen-activated protein kinases (MAPK) signal pathway on the apoptosis induction of Hep3B human hepatocarcinoma cells by a synthetic methyl jasmonate derivative (methyl 5-chloro-4,5-didehydrojasmonate, J-7). We found that treatment of Hep3B cells with J-7 markedly increased phospholylation of extracellular signal-regulated protein kinase (ERK) and c-Jun N-terminal kinase (JNK), and pretreatment an ERK-specific inhibitor, PD98059, and a JNK-specific inhibitor, SP600125, showed increased anti-proliferative action and apoptosis by J-7. The synergistic increased apoptotic events in Hep3B cells caused by blocking the ERK and JNK pathways were associated an up-regulation of death receptor 5 (DR5) and a decrease of Bid, X-linked inhibitor of apoptosis protein (XIAP) and cIAP-1 expression. Additionally, our results also indicated that the increased apoptosis by co-administration of PD98059 and SP600125 with J-7 in Hep3B cells was connected with the down-regulation of pro-caspases (-3, -8 and -9). Taken together, these findings suggest that apoptotic cell death by J-7 in Hep3B cells are associated with the activation of the ERK and JNK pathways. (Cancer Prev Res 16, 126-133, 2011)

Keywords: J-7, Hep3B, Apoptosis, ERK, JNK

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