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

Research output: Contribution to journalArticle

24 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)641-645
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume370
Issue number4
DOIs
Publication statusPublished - 2008 Jun 13

Fingerprint

Activating Transcription Factor 3
AMP-Activated Protein Kinases
JNK Mitogen-Activated Protein Kinases
Hep G2 Cells
Phosphorylation
Hepatocellular Carcinoma
Cannabinoid Receptor Antagonists
Bioactivity
Amides
Tumors
Signal Transduction
Chemical activation
AM 251
Neoplasms

Keywords

  • AM251
  • AMPK
  • ATF3
  • Cannabinoid antagonist
  • JNK

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

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title = "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",
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.",
keywords = "AM251, AMPK, ATF3, Cannabinoid antagonist, JNK",
author = "Lee, {Yun Mi} and Uhm, {Kyung Ok} and Lee, {Eun Soo} and Joseph Kwon and Sun-Hwa Park and Kim, {Hyeon Soo}",
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T1 - 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

AU - Lee, Yun Mi

AU - Uhm, Kyung Ok

AU - Lee, Eun Soo

AU - Kwon, Joseph

AU - Park, Sun-Hwa

AU - Kim, Hyeon Soo

PY - 2008/6/13

Y1 - 2008/6/13

N2 - 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.

AB - 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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KW - ATF3

KW - Cannabinoid antagonist

KW - JNK

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