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Updated: Jun 11, 2026

Methods to Study Mrp4-containing Macromolecular Complexes in the Regulation of Fibroblast Migration
Published on: May 19, 2016
Migration Stimulating Factor (MSF) promotes fibroblast migration by inhibiting AKT
Ian R Ellis1, Sarah J Jones, Yvonne Lindsay
1Unit of Cell and Molecular Biology, The Dental School, College of Medicine, Dentistry and Nursing, University of Dundee, Park Place, Dundee DD1 4HR, UK.
Abstract:
The protein kinase AKT is activated strongly by many motogenic growth factors, yet has recently been shown capable of inhibiting migration in several cell types. Here we report that treatment with Migration Stimulating Factor (MSF), a truncated form of fibronectin that promotes the migration of many cell types, inhibits AKT activity in human fibroblasts and endothelial cells. In fibroblasts, treatment with either MSF or the AKT inhibitor, Akti-1/2, stimulated migration into 3D collagen gels to a similar extent and the effects of Akti-1/2 on migration could be blocked by the expression of an inhibitor-resistant mutant, AKT1 W80A. These data indicate that MSF promotes fibroblast migration, at least in part, by inhibiting the activity of AKT.
Insights
Migration Stimulating Factor (MSF) inhibits AKT activity, promoting cell migration. This study reveals MSF
Area of Science:
- Cellular biology
- Molecular biology
- Biochemistry
Background:
- The protein kinase AKT is activated by motogenic growth factors.
- AKT can inhibit cell migration in certain cell types.
- Migration Stimulating Factor (MSF) is a fibronectin fragment promoting cell migration.
Purpose of the Study:
- To investigate the effect of MSF on AKT activity in human fibroblasts and endothelial cells.
- To determine the role of AKT inhibition in MSF-induced cell migration.
Main Methods:
- Treatment of human fibroblasts and endothelial cells with MSF.
- Assessment of AKT activity.
- Analysis of cell migration into 3D collagen gels.
- Use of AKT inhibitor (Akti-1/2) and inhibitor-resistant AKT1 W80A mutant.
Main Results:
- MSF treatment inhibited AKT activity in human fibroblasts and endothelial cells.
- Both MSF and the AKT inhibitor Akti-1/2 stimulated fibroblast migration into 3D collagen gels.
- The stimulatory effect of Akti-1/2 on migration was blocked by the AKT1 W80A mutant.
Conclusions:
- MSF promotes fibroblast migration, at least partially, by inhibiting AKT activity.
- These findings elucidate a novel mechanism for MSF-mediated cell migration.
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