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Updated: May 10, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

DYRK2 controls the epithelial-mesenchymal transition in breast cancer by degrading Snail

Rei Mimoto1, Naoe Taira, Hiroyuki Takahashi

  • 1Department of Biochemistry, The Jikei University School of Medicine, Tokyo, Japan; Department of Surgery, The Jikei University School of Medicine, Tokyo, Japan; Department of Anatomy, The Jikei University School of Medicine, Tokyo, Japan.

Cancer Letters
|June 25, 2013
PubMed

Insights

Dual specificity tyrosine-phosphorylation-regulated kinase 2 (DYRK2) degrades Snail, a key regulator of the epithelial-mesenchymal transition (EMT). Down-regulation of DYRK2 promotes breast cancer invasion and metastasis, indicating its role as a tumor suppressor.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The epithelial-mesenchymal transition (EMT) is crucial for breast cancer invasion.
  • Snail, a transcriptional repressor, drives EMT and is regulated by phosphorylation and degradation.
  • GSK3β and βTrCP mediate Snail degradation.

Purpose of the Study:

  • To identify novel regulators of Snail stability.
  • To investigate the role of DYRK2 in breast cancer progression and metastasis.

Main Methods:

  • Investigated DYRK2's role in Snail regulation using in vitro and in vivo models.
  • Assessed EMT and invasion upon DYRK2 knockdown.
  • Analyzed DYRK2 expression in human breast cancer tissues and correlated with patient outcomes.

Main Results:

  • DYRK2 was identified as a novel kinase regulating Snail stability.
  • Knockdown of DYRK2 promoted EMT and enhanced cancer invasion both in vitro and in vivo.
  • DYRK2 expression was down-regulated in human breast cancer tissues.
  • Low DYRK2 expression in tumors correlated with poorer patient outcomes.

Conclusions:

  • DYRK2 suppresses breast cancer invasion and metastasis by promoting Snail degradation.
  • DYRK2 functions as a tumor suppressor in breast cancer.
  • DYRK2 represents a potential therapeutic target for inhibiting cancer metastasis.
Keywords:
Breast cancerDYRK2E-cadherinEMTSnail

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