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

Yun Mi Lee, Kyung Ok Uhm, Eun Soo Lee, Joseph Kwon, Sun-Hwa Park, Hyeon Soo Kim

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24 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)641-645
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number4
Publication statusPublished - 2008 Jun 13



  • AM251
  • AMPK
  • ATF3
  • Cannabinoid antagonist
  • JNK

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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