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AMPK and cell proliferation--AMPK as a therapeutic target for atherosclerosis and cancer

Hiroyuki Motoshima1, Barry J Goldstein, Motoyuki Igata

  • 1Department of Metabolic Medicine, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 8554, Japan. hmoto@gpo.kumamoto-u.ac.jp

The Journal of Physiology
|April 15, 2006
PubMed

Insights

AMPK (AMP-activated protein kinase) suppresses cell proliferation by regulating cell cycle and protein synthesis. Targeting AMPK offers a therapeutic strategy for cancer and atherosclerosis.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Background:

  • AMP-activated protein kinase (AMPK) acts as a crucial cellular energy sensor in eukaryotes.
  • AMPK activation is known to inhibit cell proliferation in both normal and cancerous cells.
  • AMPK signaling involves tumor suppressor genes and counteracts growth factor signaling pathways.

Purpose of the Study:

  • To review recent advances on AMPK's role as a suppressor of cell proliferation.
  • To highlight the diverse cellular mechanisms regulated by AMPK.
  • To discuss the therapeutic potential of AMPK activation in proliferative diseases.

Main Methods:

  • Literature review of published studies on AMPK.
  • Analysis of AMPK's regulatory mechanisms on cell cycle and metabolism.
  • Examination of AMPK's interaction with key signaling pathways (e.g., mTOR, p53).

Main Results:

  • AMPK regulates cell cycle progression via the p53-p21 axis and TSC2-mTOR pathway.
  • AMPK inhibits protein synthesis and de novo fatty acid synthesis, including cholesterol pathway intermediates.
  • AMPK signaling network integrates tumor suppressors (LKB1, p53, TSC1/2) and antagonizes oncogenic pathways (PI3K/Akt, ERK).

Conclusions:

  • AMPK activation demonstrates significant tumor suppressive functions.
  • AMPK's multifaceted control over cellular events makes it a promising therapeutic target.
  • Targeting AMPK holds potential for treating proliferative diseases like cancer and atherosclerosis.

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