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Updated: Jan 27, 2026

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MEST induces Twist-1-mediated EMT through STAT3 activation in breast cancers

Min Soo Kim1, Hyun Sook Lee2,3, Yun Jae Kim2,3

  • 1Laboratory of Molecular Disease and Cell Regulation, Department of Biochemistry, School of Medicine, Gachon University, Incheon, 406-840, Korea.

Cell Death and Differentiation
|March 24, 2019
PubMed

Insights

MEST protein promotes breast cancer metastasis by activating the IL-6/JAK/STAT3/Twist-1 pathway and inducing epithelial-mesenchymal transition (EMT). Targeting MEST could prevent tumor spread.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Loss of imprinting of MEST is linked to cancer via promoter switching.
  • MEST's role in tumor growth and metastasis requires further elucidation.

Purpose of the Study:

  • To investigate MEST's function in breast cancer metastasis.
  • To identify the molecular mechanisms underlying MEST-driven metastasis.

Main Methods:

  • Analysis of MEST expression in breast cancer patients.
  • Investigating MEST's effect on epithelial-mesenchymal transition (EMT).
  • Studying the IL-6/JAK/STAT3/Twist-1 signaling pathway and MEST's role in metastasis using experimental models.

Main Results:

  • Elevated MEST expression correlates with breast cancer pathogenesis.
  • MEST enhances breast cancer cell metastatic potential by inducing EMT via the IL-6/JAK/STAT3/Twist-1 pathway.
  • MEST activates STAT3, promoting Twist-1 expression and EMT.
  • The C-terminal region of MEST is crucial for JAK2/STAT3 complex formation and STAT3 activation.
  • MEST is essential for metastasis in experimental models.

Conclusions:

  • MEST is a key regulator of breast cancer metastasis through the IL-6/JAK/STAT3/Twist-1 pathway.
  • MEST drives EMT and promotes tumor spread.
  • MEST represents a potential therapeutic target for preventing breast cancer metastasis.

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