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Mesenchymal cells reactivate Snail1 expression to drive three-dimensional invasion programs.
R Grant Rowe1, Xiao-Yan Li, Yuexian Hu
1Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
The Journal of Cell Biology
|February 4, 2009
Summary
The zinc-finger transcription factor Snail1 regulates mesenchymal cell function after differentiation. Snail1 deficiency impairs fibroblast invasion and angiogenesis, highlighting its role beyond epithelial-mesenchymal transition (EMT).
Area of Science:
- Cell Biology
- Developmental Biology
- Molecular Biology
Background:
- Epithelial-mesenchymal transition (EMT) is crucial for mesodermal differentiation.
- Snail1 (zinc-finger transcription factor) induces EMT and cellular reprogramming.
- Snail1's role in terminally differentiated mesenchymal cells is unknown.
Purpose of the Study:
- To investigate Snail1's function in normal mesenchymal cells.
- To determine if Snail1 regulates post-differentiation mesenchymal cell behavior.
Main Methods:
- Utilized a Snai1 conditional knockout mouse model.
- Analyzed gene expression in Snail1-deficient fibroblasts within a 3D extracellular matrix.
- Assessed fibroblast invasive potential and angiogenesis using the chick chorioallantoic membrane assay.
Main Results:
- Snail1 deficiency in fibroblasts caused global gene expression alterations.
- Snail1-deficient fibroblasts showed impaired membrane type-1 matrix metalloproteinase (MT1-MMP)-dependent invasion.
- These fibroblasts lacked tissue-invasive potential and failed to induce angiogenesis in vivo.
Conclusions:
- Snail1 is a key regulator of normal mesenchymal cell function post-differentiation.
- Snail1 controls fibroblast invasiveness and the induction of angiogenesis.
- These findings reveal novel roles for Snail1 beyond its established function in EMT.
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