AM251 suppresses the viability of HepG2 cells through the AMPK (AMP-activated protein kinase)-JNK (c-Jun N-terminal kinase)-ATF3 (activating transcription factor 3) pathway
- Authors
- Lee, Yun Mi; Uhm, Kyung-Ok; Lee, Eun Soo; Kwon, Joseph; Park, Sun Hwa; Kim, Hyeon Soo
- Issue Date
- 13-6월-2008
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- AMPK; AM251; cannabinoid antagonist; JNK; ATF3
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.370, no.4, pp.641 - 645
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 370
- Number
- 4
- Start Page
- 641
- End Page
- 645
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/123380
- DOI
- 10.1016/j.bbrc.2008.04.003
- ISSN
- 0006-291X
- 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. (c) 2008 Published by Elsevier Inc.
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Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
- Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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