Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1935419 | Biochemical and Biophysical Research Communications | 2008 | 5 Pages |
Abstract
AM251, a cannabinoid antagonist, has various biological activities. In this study, we found that AM251 suppressed the viability of hepatoma HepG2 cells and also increased phosphorylation of JNK (c-jun N-terminal kinase) and ATF3 (activating transcription factor 3). In addition, AM251 phosphorylated AMPK (AMP-activated protein kinase) in a time and dose-dependent manner. Inhibition of AMPK blocked AM251-induced JNK/ATF3 phosphorylation. Expression of AMPK or treatment with AICAR (5-aminoimidazole-4-carboxy-amide-1-d-ribofuranoside), an AMPK activator, activated the JNK/ATF3 pathways. Together, these results suggest that AM251 may have anti-tumor effects in hepatoma through activation of the AMPK–JNK–ATF3 signal pathway.
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Authors
Yun Mi Lee, Kyung-Ok Uhm, Eun Soo Lee, Joseph Kwon, Sun Hwa Park, Hyeon Soo Kim,