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14-3-3σ regulates β-catenin-mediated mouse embryonic stem cell proliferation by sequestering GSK-3β

Tzu-Ching Chang1, Chia-Chia Liu, En-Wei Hsing

  • 1Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.

Plos One
|July 7, 2012
PubMed
Abstract

Insights

14-3-3σ protein promotes embryonic stem cell proliferation by regulating GSK-3β and Wnt signaling pathways. This finding identifies 14-3-3σ as a potential target for enhancing stem cell expansion in regenerative medicine.

Area of Science:

  • Stem cell biology
  • Molecular mechanisms of cell proliferation
  • Protein-protein interactions

Background:

  • Embryonic stem cells (ESCs) are a vital source for regenerative medicine.
  • Understanding ESC proliferation regulation is crucial.
  • The role of 14-3-3 proteins in ESCs was previously unknown.

Purpose of the Study:

  • To investigate the function of 14-3-3 proteins in mouse ESC proliferation.
  • To elucidate the molecular mechanisms by which 14-3-3 proteins regulate ESC growth.

Main Methods:

  • Detection of 14-3-3 isoforms in mouse ESCs.
  • Selective knockdown and overexpression of 14-3-3σ using siRNA and transfection.
  • Analysis of β-catenin and GSK-3β phosphorylation and interactions.
  • Assessment of Wnt signaling pathway activity.

Main Results:

  • All seven 14-3-3 isoforms are present in mouse ESCs.
  • 14-3-3σ knockdown reduced ESC proliferation; 14-3-3σ overexpression enhanced it.
  • 14-3-3σ binds GSK-3β, increasing its phosphorylation and disrupting β-catenin degradation.
  • 14-3-3σ enhances Wnt-induced signaling and rescues retinoid acid-induced growth arrest.

Conclusions:

  • 14-3-3σ is a key regulator of mouse ESC proliferation.
  • It functions by binding and sequestering phosphorylated GSK-3β, impacting Wnt signaling.
  • 14-3-3σ represents a novel therapeutic target for ESC expansion.

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