Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 110, Issue 3, Pages 581-588Publisher
WILEY
DOI: 10.1002/jcb.22551
Keywords
ST13; HIP; ASK1; JNK; APOPTOSIS
Categories
Funding
- National Nature Science Foundation of China [30623003, 30800570]
- Science and Technology Commission of Shanghai Municipality [06DZ22032]
- National Basic Research Program of China [2004 CB51804]
- Hi-Tech Research Development Program of China
- Zhejiang Sci-Tech University [0616033]
- Shanghai Leading Academic [B110]
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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 (ASK I) 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 ASK! 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. (C) 2010 Wiley-Liss, Inc.
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