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Updated: May 25, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

BMK1 kinase suppresses epithelial-mesenchymal transition through the Akt/GSK3β signaling pathway

Runqiang Chen1, Qingkai Yang, Jiing-Dwan Lee

  • 1Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California 92037, USA.

Cancer Research
|January 28, 2012
PubMed

Insights

Mitogen-activated protein kinase BMK1 signaling suppresses epithelial-mesenchymal transition (EMT), a key process in cancer metastasis. BMK1 activation enhances cell adhesion and reduces motility, while its inhibition promotes metastasis by increasing nuclear Snail accumulation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Epithelial-mesenchymal transition (EMT) is critical for cancer metastasis.
  • Mitogen-activated protein (MAP) kinases like ERK, JNK, and p38 are implicated in EMT.
  • The role of MAP kinase BMK1 in EMT has not been previously investigated.

Purpose of the Study:

  • To investigate the role of BMK1 signaling in regulating EMT.
  • To elucidate the molecular mechanisms by which BMK1 influences EMT and metastasis.

Main Methods:

  • Investigated BMK1 signaling effects on E-cadherin, mesenchymal markers, and cell motility.
  • Analyzed nuclear Snail accumulation and its regulation by Akt/GSK3β and mTOR signaling.
  • Assessed the impact of BMK1 depletion on in vivo metastasis.

Main Results:

  • BMK1 signaling suppresses EMT by augmenting cell-cell adhesion and reducing cell motility.
  • BMK1 depletion leads to increased nuclear Snail accumulation via mTOR/Akt pathway activation.
  • BMK1 inhibition promotes cancer metastasis in vivo.

Conclusions:

  • BMK1 signaling acts as a suppressor of EMT and cancer metastasis.
  • A novel mechanism of EMT control involves BMK1-mediated inhibition of mTOR/Akt signaling.
  • Targeting BMK1 may offer a therapeutic strategy to inhibit cancer metastasis.

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