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Journal of Cell Science 115, 3193-3206 (2002)
© 2002 The Company of Biologists Limited

Research Article

p38 mitogen-activated protein kinase is required for TGFß-mediated fibroblastic transdifferentiation and cell migration

Andrei V. Bakin1, Cammie Rinehart1, Anne K. Tomlinson1 and Carlos L. Arteaga1,2,3,*

1 Department of Medicine, Vanderbilt University School of Medicine, 777 Preston Research Building, Nashville, TN 37232, USA
2 Department of Cancer Biology, Vanderbilt University School of Medicine, 777 Preston Research Building, Nashville, TN 37232, USA
3 Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, 777 Preston Research Building, Nashville, TN 37232, USA

* Author for correspondence (e-mail: carlos.arteaga{at}mcmail.vanderbilt.edu )

Accepted 23 April 2002

Transforming growth factor ß (TGFß) contributes to tumor progression by inducing an epithelial to mesenchymal transdifferentiation (EMT) and cell migration. We found that TGFß-induced EMT was blocked by inhibiting activation of p38 mitogen-activated protein kinase (MAPK) with H-7, a protein kinase C inhibitor, and with SB202190, a direct inhibitor of p38MAPK. Inhibition of the p38MAPK pathway affected TGFß-mediated phosphorylation of ATF2, but did not inhibit phosphorylation of Smad2. SB202190 impaired TGFß-mediated changes in cell shape and reorganization of the actin cytoskeleton. Forced expression of dominant-negative (DN) MAPK kinase 3 (MKK3) inhibited TGFß-mediated activation of p38MAPK and EMT. Expression of DN-p38{alpha} impaired TGFß-induced EMT. Inhibition of p38MAPK blocked TGFß-induced migration of non-tumor and tumor mammary epithelial cells. TGFß induced activation of the p38MAPK pathway within 15 minutes. Expression of TGFß type II (TßRII) and type I (TßRI/Alk5) kinase-inactive receptors blocked EMT and activation of p38MAPK, whereas expression of constitutively active Alk5-T204D resulted in EMT and phosphorylation of MKK3/6 and p38MAPK. Finally, dominant-negative Rac1N17 blocked TGFß-induced activation of the p38MAPK pathway and EMT, suggesting that Rac1 mediates activation of the p38MAPK pathway. These studies suggest that the p38MAPK pathway is required for TGFß-mediated EMT and cell migration.

Key words: p38MAPK, TGFß, Epithelial-mesenchymal transition, Cell migration, Rac1


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 J. Am. Soc. Nephrol.Home page
H. Ha and H. B. Lee
Reactive Oxygen Species and Matrix Remodeling in Diabetic Kidney
J. Am. Soc. Nephrol., August 1, 2003; 14(90003): S246 - 249.
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 Mol. Biol. CellHome page
R. C. Bates and A. M. Mercurio
Tumor Necrosis Factor-{alpha} Stimulates the Epithelial-to-Mesenchymal Transition of Human Colonic Organoids
Mol. Biol. Cell, May 1, 2003; 14(5): 1790 - 1800.
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N. Dumont, A. V. Bakin, and C. L. Arteaga
Autocrine Transforming Growth Factor-beta Signaling Mediates Smad-independent Motility in Human Cancer Cells
J. Biol. Chem., January 24, 2003; 278(5): 3275 - 3285.
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