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Integrin β1 Signaling Is Necessary for Transforming Growth Factor-β Activation of p38MAPK and Epithelial Plasticity
Open accessAbstract
Transforming growth factor-beta (TGF-beta) can induce epithelial to mesenchymal transdifferentiation (EMT) in mammary epithelial cells. TGF-beta-mediated EMT involves the stimulation of a number of signaling pathways by the sequential binding of the type II and type I serine/threonine kinase receptors, respectively. Integrins comprise a family of heterodimeric extracellular matrix receptors that mediate cell adhesion and intracellular signaling, hence making them crucial for EMT progression. In light of substantial evidence indicating TGF-beta regulation of various beta(1) integrins and their extracellular matrix ligands, we examined the cross-talk between the TGF-beta and integrin signal transduction pathways. Using an inducible system for the expression of a cytoplasmically truncated dominant negative TGF-beta type II receptor, we blocked TGF-beta-mediated growth inhibition, transcriptional activation, and EMT progression. Dominant negative TGF-beta type II receptor expression inhibited TGF-beta signaling to the SMAD and AKT pathways, but did not block TGF-beta-mediated p38MAPK activation. Interestingly, blocking integrin beta(1) function inhibited TGF-beta-mediated p38MAPK activation and EMT progression. Limiting p38MAPK activity through the expression of a dominant negative-p38MAPK also blocked TGF-beta-mediated EMT. In summary, TGF-beta-mediated p38MAPK activation is dependent on functional integrin beta(1), and p38MAPK activity is required but is not sufficient to induce EMT.
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Cites
Weaver, V. M., Petersen, O. W., Wang, F., Larabell, C. A., Briand, P., Damsky, C., & Bissell, M. J. (1997) · The Journal of Cell Biology · doi:10.1083/jcb.137.1.231 · Cited by 1,483
Cell adhesion protein receptors as targets for transforming growth factor-$beta; action
IGNOTZ, R. (1987) · Cell · doi:10.1016/0092-8674(87)90146-2 · Cited by 485
Cited by
The basics of epithelial-mesenchymal transition
Kalluri, R., & Weinberg, R. A. (2009) · Journal of Clinical Investigation · doi:10.1172/jci39104 · Cited by 10,196
Signaling mechanisms of the epithelial-mesenchymal transition
Gonzalez, D. M., & Medici, D. (2014) · Science Signaling · doi:10.1126/scisignal.2005189 · Cited by 1,721
Integrin–TGF‐β crosstalk in fibrosis, cancer and wound healing
Margadant, C., & Sonnenberg, A. (2010) · The EMBO Reports · doi:10.1038/embor.2009.276 · Cited by 653
Hayashida, T., de Caestecker, M., & Schnaper, H. W. (2003) · The FASEB Journal · doi:10.1096/fj.03-0037fje · Cited by 361
Horowitz, J. C., Lee, D. Y., Waghray, M., Keshamouni, V. G., Thomas, P. E., Zhang, H., Cui, Z., & Thannickal, V. J. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m306248200 · Cited by 239
Metadata
- Authors
- Bhowmick, N. A., Zent, R., Ghiassi, M., McDonnell, M., & Moses, H. L.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2001-12
- Volume
- 276
- Issue
- 50
- Pages
- 46707-46713
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1999614450
- Cited by
- 388
- References
- 2
- FWCI
- 5.43
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Bhowmick, N. A., Zent, R., Ghiassi, M., McDonnell, M., & Moses, H. L. (2001). Integrin β1 Signaling Is Necessary for Transforming Growth Factor-β Activation of p38MAPK and Epithelial Plasticity. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m106176200
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