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Crosstalk from survival to necrotic death coexists in DU-145 cells by curcumin treatment: Inhibition of apoptosis by caspase degradation.

 Dongxu Kang  ;  Wungki Park  ;  Seungha Lee  ;  Joo-Hang Kim  ;  Jae J. Song 
 CELLULAR SIGNALLING, Vol.25(5) : 1288-1300, 2013 
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Issue Date
Curcumin ; Autophagy ; Necrosis ; ROS ; Caspase ; LC3II
Curcumin as an anticancer agent was investigated in regards to its ability to regulate the switching of cancer cells from survival to necrotic cell death. At higher concentrations, curcumin induced ROS production leading to JNK and p38 phosphorylation in DU-145 prostate cancer cells. Of the MAP kinases, ERK or p38/JNK were phosphorylated earlier during curcumin treatment, and were responsible for curcumin-induced cell survival at early time of treatment with the help of phosphorylated Akt, while significant amounts of ROS production in later periods stimulated cell death with caspase degradation. In addition to autophagic signaling, necrosis was dominant with little apoptotic cell death. Caspase activation was completely prohibited by procaspase degradation, which contributed to curcumin-induced early necrosis. At the later incubation period (24 h), cytotoxicity caused by curcumin peaked, at which time survival or proliferation signals, such as phosphorylated Akt and phosphorylated ERK, was almost completely diminished. Curcumin-induced ROS were shown to function, biphasically depending on the incubation period; facilitating survival, in the earlier incubation period, and necrotic death in the later. Based on all of these results, we concluded that curcumin contributes to a complex signaling network, affecting cell survival and necrotic cell death, which in turn could inhibit apoptotic cell death.
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Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Institute for Cancer Research (암연구소) > 1. Journal Papers
Yonsei Authors
Kim, Joo Hang(김주항)
Song, Jae Jin(송재진) ORCID logo https://orcid.org/0000-0001-8183-9550
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