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Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

AMP-activated protein kinase is required for induction of apoptosis and epithelial-to-mesenchymal transition

Xunde Wang1, Xinchao Pan, Jianguo Song

  • 1Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue-Yang Road, Shanghai 200031, China.

Cellular Signalling
|July 24, 2010
PubMed

Insights

AMP-activated protein kinase (AMPK) regulates cellular energy. This study reveals AMPK activation by TGF-beta1 promotes apoptosis and EMT by modulating Smad3 transcriptional activity in hepatocytes.

Area of Science:

  • Cellular Biology
  • Molecular Signaling
  • Biochemistry

Background:

  • AMP-activated protein kinase (AMPK) is crucial for cellular energy homeostasis.
  • Limited knowledge exists regarding AMPK's function in other cellular processes.
  • Transforming growth factor-beta1 (TGF-beta1) is a key signaling molecule with diverse cellular effects.

Purpose of the Study:

  • To investigate the role of AMPK in TGF-beta1-induced cellular responses.
  • To determine if AMPK activation is involved in TGF-beta1-mediated apoptosis and epithelial-mesenchymal transition (EMT).
  • To elucidate the molecular mechanisms linking AMPK to TGF-beta1 signaling.

Main Methods:

  • Activation of AMPK in mouse hepatocytes.
  • Inhibition of AMPK using Compound C, a selective AMPK-alpha inhibitor.
  • Overexpression of a dominant-negative AMPK-alpha subunit in AML12 cells.
  • Assessment of TGF-beta1-induced apoptosis and EMT.
  • Measurement of TGF-beta1-induced Smad3 transcriptional activity.

Main Results:

  • TGF-beta1 activated AMPK-alpha in mouse hepatocytes.
  • Inhibition of AMPK suppressed TGF-beta1-induced apoptosis and EMT.
  • Overexpression of dominant-negative AMPK-alpha also inhibited TGF-beta1-induced EMT and apoptosis.
  • AMPK inhibition attenuated TGF-beta1-induced Smad3 transcriptional activity.

Conclusions:

  • AMPK plays a significant role in mediating TGF-beta1-induced apoptosis and EMT.
  • AMPK modulates Smad3 transcriptional activity, a key pathway in TGF-beta1 signaling.
  • This study identifies AMPK as a novel regulator of TGF-beta1-driven cellular processes.

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