Abstract
It has been shown that acetylcholinesterase (AChE) expression was induced during apoptosis and the anti-sense oligonucleotides and siRNA of AChE may prevent apoptosis in various cell types. However, the mechanisms underlying AChE upregulation remain elusive. We demonstrated here that c-Jun NH2-terminal kinase (JNK) could mediate AChE expression. In this study, both etoposide and excisanin A, two anticancer agents, induced apoptosis in colon cancer cell line SW620 as determined by Annexin V staining, the cleavage of caspase-3 and the proteolytic degradation of poly (ADP-ribose) polymerase (PARP). The results showed that both the agents upregulated AChE in SW620 cells. In the meantime, JNK was also activated and the expression and phosphorylation of c-Jun increased in SW620 cells exposed to the two agents. The induced AChE mRNA and protein expression could be blocked by SP600125, a specific inhibitor of SAPK/JNK, and small interfering RNA directed against JNK1/2. Transfection with adenovirus-mediated dominant negative c-Jun also blocked the upregulation of AChE expression. Together, these results suggest that AChE expression may be mediated by the activation of JNK pathway during apoptosis through a c-Jun-dependent mechanism.
Original language | English |
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Pages (from-to) | 7070-7077 |
Number of pages | 8 |
Journal | Oncogene |
Volume | 25 |
Issue number | 53 |
DOIs | |
Publication status | Published - 9 Nov 2006 |
Externally published | Yes |
Keywords
- Acetylcholinesterase (AChE)
- Apoptosis
- c-Jun NH2-terminal kinase (JNK)
- Extracellular signal regulated kinase (ERK)
- Mitogen-activated protein kinase (MAPK)
ASJC Scopus subject areas
- Molecular Biology
- Genetics
- Cancer Research