کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2602948 1133802 2010 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Evodiamine-induced human melanoma A375-S2 cell death was mediated by PI3K/Akt/caspase and Fas-L/NF-κB signaling pathways and augmented by ubiquitin–proteasome inhibition
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
Evodiamine-induced human melanoma A375-S2 cell death was mediated by PI3K/Akt/caspase and Fas-L/NF-κB signaling pathways and augmented by ubiquitin–proteasome inhibition
چکیده انگلیسی

Evodiamine, a major alkaloidal component of Evodiae fructus exhibits anti-tumor activities. We have previously reported that evodiamine has a marked inhibitory effect on IL-1 sensitive human melanoma A375-S2 cells proliferation, and this action might be through inactivation of PI3K signaling. However, the detailed molecular mechanisms of evodiamine-induced cell death remains poorly understood. In present study, we further confirmed that Akt is the main effector molecule involved in this pathway. Evodiamine also led to IκBα phosphorylation and degradation that reflect translocation of NF-κB. Pretreatment of A375-S2 cells with ubiquitin–proteasome inhibitor MG132 was shown to aggregate the evodiamine caused cell death at 24 h. In addition, MG132 reduced ERK phosphorylation, increased caspase-3 activation, Fas-L expression and Bcl-2 cleavage in evodiamine-treated A375-S2 cells. These results suggested the PI3K/Akt/caspase and Fas-L/NF-κB signaling pathways might account for the responses of A375-S2 cell death induced by evodiamine, and these signals could be augmented by ubiquitin–proteasome pathway.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology in Vitro - Volume 24, Issue 3, April 2010, Pages 898–904
نویسندگان
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