Related Experiment Video

Updated: Aug 5, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

Targeting the Extracellular Signal-Regulated Kinase 5-Cellular Jun-Vimentin Axis to Inhibit Epithelial-Mesenchymal

Chia-Chi Chen1,2,3, Shu-Jyuan Chang1, Cheng-Loong Liang4

  • 1Graduate Institute of Clinical Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.

International Journal of Medical Sciences
|July 29, 2026
PubMed

Insights

High extracellular signal-regulated kinase 5 (ERK5) expression drives triple-negative breast cancer (TNBC) progression and metastasis. Targeting the ERK5/c-JUN/vimentin pathway may offer new therapeutic strategies for TNBC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) is aggressive with high metastasis risk.
  • Extracellular signal-regulated kinase 5 (ERK5) promotes tumor progression, but its role in TNBC epithelial-mesenchymal transition (EMT) is unclear.

Purpose of the Study:

  • To investigate the role of ERK5 in TNBC progression, metastasis, and EMT.
  • To identify potential therapeutic targets within the ERK5 signaling pathway.

Main Methods:

  • Analysis of 117 TNBC patient data for ERK5 expression and survival correlation.
  • RNA sequencing of TNBC cell lines with ERK5 knockdown.
  • In vivo studies using a mouse xenograft model.
  • Investigation of ERK5's interaction with c-JUN and vimentin promoter.

Main Results:

  • High ERK5 expression correlated with tumor progression and poorer survival in TNBC patients.
  • ERK5 knockdown suppressed tumor proliferation, metastasis, and EMT markers in vitro and in vivo.
  • ERK5 regulates c-JUN recruitment to the vimentin promoter, modulating vimentin expression.

Conclusions:

  • ERK5 promotes TNBC metastasis by regulating the ERK5/c-JUN/vimentin axis.
  • This pathway is a potential therapeutic target for improving TNBC patient outcomes.
Keywords:
ERK5JunTNBCVimentinepithelial-mesenchymal transitionmetastasis

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