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- Edlund, SofiaUppsala universitet,Ludwiginstitutet för cancerforskning (author)
Transforming growth factor-beta-induced mobilization of actin cytoskeleton required signaling by small GTPases Cdc42 and RhoA
- Article/chapterEnglish2002
Publisher, publication year, extent ...
- The American Society for Cell Biology,2002
- printrdacarrier
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- LIBRIS-ID:oai:DiVA.org:uu-90259
- https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-90259URI
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- Language:English
- Summary in:English
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- Transforming growth factor-beta (TGF-beta) is a potent regulator of cell growth and differentiation in many cell types. The Smad signaling pathway constitutes a main signal transduction route downstream of TGF-beta receptors. We studied TGF-beta-induced rearrangements of the actin filament system and found that TGF-beta 1 treatment of PC-3U human prostate carcinoma cells resulted in a rapid formation of lamellipodia. Interestingly, this response was shown to be independent of the Smad signaling pathway; instead, it required the activity of the Rho GTPases Cdc42 and RhoA, because ectopic expression of dominant negative mutant Cdc42 and RhoA abrogated the response. Long-term stimulation with TGF-beta 1 resulted in an assembly of stress fibers; this response required both signaling via Cdc42 and RhoA, and Smad proteins. A known downstream effector of Cdc42 is p38(MAPK); treatment of the cells with the p38(MAPK) inhibitor 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(pyridyl)1H-imidazole (SB203580), as well as ectopic expression of a kinase-inactive p38(MAPK), abrogated the TGF-beta-induced actin reorganization. Moreover, treatment of cells with the inhibitors of the RhoA target-protein Rho-associated coiled-coil kinase (+)-R-trans-4-(aminoethyl)-N-(4-pyridyl) cyclohexanecarboxamide (Y-27632) and 1-5(-isoquinolinesulfonyl)homopiperazine (HA-1077), as well as ectopic expression of kinase-inactive Rho coiled-coil kinase-1, abrogated the TGF-beta 1-induced formation of stress fibers. Collectively, these data indicate that TGF-beta-induced membrane ruffles occur via Rho GTPase-dependent pathways, whereas long-term effects require cooperation between Smad and Rho GTPase signaling pathways.
Subject headings and genre
- Actins/*metabolism
- Amides/pharmacology
- Animals
- Cell Surface Extensions/metabolism
- Cytoskeleton/drug effects/*metabolism
- DNA-Binding Proteins/genetics/metabolism
- Enzyme Inhibitors/pharmacology
- Humans
- Imidazoles/pharmacology
- Intracellular Signaling Peptides and Proteins
- Mitogen-Activated Protein Kinases/antagonists & inhibitors/genetics/metabolism
- Protein-Serine-Threonine Kinases/antagonists & inhibitors/genetics/metabolism
- Pyridines/pharmacology
- Rats
- Recombinant Fusion Proteins/metabolism
- Signal Transduction/*physiology
- Smad4 Protein
- Stress Fibers/metabolism
- Trans-Activators/genetics/metabolism
- Transforming Growth Factor beta/*metabolism
- Tumor Cells; Cultured
- cdc42 GTP-Binding Protein/*metabolism
- p38 Mitogen-Activated Protein Kinases
- rac1 GTP-Binding Protein/metabolism
- rhoA GTP-Binding Protein/*metabolism
- MEDICINE
- MEDICIN
Added entries (persons, corporate bodies, meetings, titles ...)
- Landström, MaréneUppsala universitet,Ludwiginstitutet för cancerforskning(Swepub:uu)mareland (author)
- Heldin, Carl-HenrikUppsala universitet,Ludwiginstitutet för cancerforskning(Swepub:uu)carlheld (author)
- Aspenström, PontusUppsala universitet,Ludwiginstitutet för cancerforskning(Swepub:uu)pontaspe (author)
- Uppsala universitetLudwiginstitutet för cancerforskning (creator_code:org_t)
Related titles
- In:Molecular Biology of the Cell: The American Society for Cell Biology13:3, s. 902-9141059-15241939-4586
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