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Updated: Aug 9, 2026

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

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Regulation of vimentin by SIP1 in human epithelial breast tumor cells

S Bindels1, M Mestdagt, C Vandewalle

  • 1Laboratory of Tumor and Developmental Biology, Center for Biomedical Integrated Genoproteomics, University of Liège, CHU Sart-Tilman, Liège, Belgium.

Oncogene
|March 29, 2006
PubMed

Insights

Smad interacting protein-1 (SIP1) promotes breast tumor cell migration and invasion by regulating vimentin expression during epithelial-to-mesenchymal transitions (EMTs). This pathway may drive breast cancer metastasis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Epithelial-to-mesenchymal transition (EMT) is crucial for tumor cell migration and invasion.
  • Smad interacting protein-1 (SIP1; ZEB2) and vimentin are key markers often upregulated during EMT.

Purpose of the Study:

  • To investigate the role of SIP1 in regulating vimentin expression during EMT in breast cancer.
  • To understand SIP1's contribution to breast tumor cell migration and invasion.

Main Methods:

  • Analysis of SIP1 and vimentin expression in breast tumor cell lines.
  • Cell migration assays using MCF10A cells with SIP1 modulation (transfection and RNAi).
  • Assessment of vimentin mRNA and protein levels.
  • TOP-FLASH reporter assay to evaluate the beta-catenin/TCF pathway.

Main Results:

  • SIP1 and vimentin were exclusively expressed in invasive breast tumor cell lines.
  • SIP1 induction correlated with vimentin expression and enhanced migration in MCF10A cells.
  • SIP1 inhibition reduced vimentin expression and cell migration.
  • SIP1 did not activate the beta-catenin/TCF pathway.

Conclusions:

  • SIP1 plays a significant role in regulating vimentin expression during EMT in breast cancer.
  • This SIP1-vimentin pathway contributes to breast tumor cell migration and invasion.
  • The findings suggest SIP1 as a potential therapeutic target for inhibiting breast cancer metastasis.

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