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Transcriptional suppression of AMPKα1 promotes breast cancer metastasis upon oncogene activation

Yong Yi1, Deshi Chen1, Juan Ao1

  • 1Center of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.

Proceedings of the National Academy of Sciences of the United States of America
|March 21, 2020
PubMed

Insights

AMP-activated protein kinase alpha 1 (AMPKα1) transcription is suppressed in breast cancer, promoting metastasis. Restoring AMPKα1 levels inhibits cancer spread by maintaining cell adhesion.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cellular Metabolism

Background:

  • AMP-activated protein kinase (AMPK) is a key energy sensor crucial for metabolic homeostasis.
  • Dysregulated AMPK activity or stability is linked to metabolic disorders and tumor development.
  • The role of AMPK transcription regulation in cancer metastasis is not well understood.

Purpose of the Study:

  • To investigate the role of AMPK transcription regulation in human breast cancer metastasis.
  • To determine the impact of AMPKα1 down-regulation on cell adhesion and tumor progression.

Main Methods:

  • Analysis of AMPKα1 expression in advanced human breast cancer tissues.
  • Investigating the effect of PI3K/HER2 activation on AMPKα1 transcription via ΔNp63α.
  • Assessing the impact of AMPKα1 ablation or inhibition on cell-cell adhesion, invasion, and metastasis in vitro and in vivo.

Main Results:

  • AMPKα1 expression is reduced in advanced breast cancer, correlating with poor clinical outcomes.
  • PI3K and HER2 activation, mediated by ΔNp63α, inhibits AMPKα1 transcription.
  • AMPKα1 loss disrupts E-cadherin-mediated cell adhesion and enhances tumor metastasis.
  • Restoring AMPKα1 expression reverses these pro-metastatic effects.

Conclusions:

  • Transcriptional control represents a significant regulatory mechanism for AMPK.
  • AMPKα1 plays a critical role in maintaining cell-cell adhesion and suppressing cancer metastasis.
  • Targeting AMPKα1 transcription may offer a therapeutic strategy for breast cancer metastasis.
Keywords:
AMPKcancer metastasiscell adhesiononcogenic signalingΔNp63α

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