Evodiamine induced human melanoma A375-S2 cell death partially through interleukin 1 mediated pathway.
We have reported that caspase cascade accompanied by the regulation of Bax/Bcl-2 and MAPK signaling were involved in evodiamine-induced A375-S2 cell death. In this study, pretreatment with interleukin 1 (IL-1) receptor antagonist (IL-1Ra) rescued the cell viability loss and reversed the ratio of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells induced by evodiamine. IL-1Ra was capable of attenuating the expression of Fas-ligand (Fas-L) and the cleavage of procaspas-8 and -3 caused by evodiamine. Subsequently, IL-1Ra reduced evodiamine-induced DNA degradation, p53 activation and up-regulation of Bax/Bcl-2 ratio. However, IL-1Ra attenuated the enhanced phosphorylation level of p38 mitogen- activated protein kinase ( p38 MAPK) without affecting extracellular signal- regulated protein kinase ( ERK) inactivation induced by evodiamine. In conclusion, IL-1-induced death cascade in melanoma A375-S2 cell might be one of the targets for natural product evodiamine, and increased Fas-L expression via IL-1 mediated pathway stands at the initiation phase, leading to consequent events that culminate in the death of the cells.[1]References
- Evodiamine induced human melanoma A375-S2 cell death partially through interleukin 1 mediated pathway. Wang, C., Wang, M.W., Tashiro, S., Onodera, S., Ikejima, T. Biol. Pharm. Bull. (2005) [Pubmed]
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