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• W2040231619 endingPage "1106" @default.
• W2040231619 startingPage "1101" @default.
• W2040231619 abstract "Transforming growth factor-beta (TGF-β) is a multifunctional cytokine involved in the regulation of cell proliferation, differentiation, and survival. Malignant tumour cells often do not respond to TGF-β by growth inhibition, but retain responsiveness to cytokine in regulating extracellular matrix deposition, cell adhesion, and migration. We demonstrated that TGF-β1 does not affect viability or proliferation of human glioblastoma T98G, but increases transcriptional responses exemplified by induction of MMP-9 expression. TGF-β receptors were functional in T98G glioblastoma cells leading to SMAD3/SMAD4 nuclear translocation and activation of SMAD-dependent promoter. In parallel, a selective activation of p38 MAPK, and phosphorylation of its substrates: ATF2 and c-Jun proteins were followed by a transient activation of AP-1 transcription factor. Surprisingly, an inhibition of p38 MAPK with a specific inhibitor, SB202190, abolished TGF-inducible activation of Smad-dependent promoter and decreased Smad2 phosphorylation. It suggests an unexpected interaction between Smad and p38 MAPK pathways in TGF-β1-induced signalling." @default.
• W2040231619 created "2016-06-24" @default.
• W2040231619 creator A5018074276 @default.
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• W2040231619 date "2007-03-01" @default.
• W2040231619 modified "2023-09-27" @default.
• W2040231619 title "Cross-talk between Smad and p38 MAPK signalling in transforming growth factor β signal transduction in human glioblastoma cells" @default.
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• W2040231619 doi "https://doi.org/10.1016/j.bbrc.2007.01.113" @default.
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