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ASK1–JNK signaling cascade mediates Ad‐ST13‐induced apoptosis in colorectal HCT116 cells
Author(s) -
Yang Min,
Yu Mingcan,
Guan Dongyin,
Gu Jinfa,
Cao Xin,
Wang Weiyun,
Zheng Shu,
Xu Yingying,
Shen Zonghou,
Liu Xinyuan
Publication year - 2010
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.22551
Subject(s) - ask1 , protein kinase r , kinase , microbiology and biotechnology , cyclin dependent kinase 9 , cancer research , cyclin dependent kinase 2 , mapk/erk pathway , apoptosis , map kinase kinase kinase , signal transduction , protein kinase a , biology , chemistry , biochemistry
ST13, a co‐factor of heat shock protein, has shown potential antitumor efficacy for colorectal cancer in our previous study. However, the molecular mechanisms governing ST13‐induced apoptosis are poorly understood. Here, we demonstrate that Ad‐ST13 (ST13 mediated by adenovirus) activates apoptosis signal‐regulated kinase (ASK1) and c‐Jun N‐terminal kinase (JNK) but not p38 (mitogen‐activated protein kinase) in human colorectal HCT116 cells. Ad‐ST13 also increases extracellular‐regulated kinase (ERK) phosphorylation levels, but the change is due to adenovirus replication. Overexpression of ST13 also increases the transcription activity of AP‐1. Blocking ASK1–JNK pathway affects Ad‐ST13‐mediated colorectal cell apoptosis, decreases the release of cytochrome c in cytoplasm and caspase activation. Because ASK1 is known to contain a tetratricopeptide repeat (TPR)‐acceptor site and ST13 has TPR domain, we found the interaction between ST13 and ASK1. These results strongly indicate Ad‐ST13 triggers colorectal cell apoptosis via ASK1–JNK signaling cascade. J. Cell. Biochem. 110: 581–588, 2010. © 2010 Wiley‐Liss, Inc.