Although much evidence has demonstrated that TGF-β1 promotes glioma cell motility and induces the expression of extracellular matrix proteins, the effects of TGF-β1 on Schwann cell migration has not yet been studied.
Evidence suggests that glioma stem cells (GSCs), maintained by the transforming growth factor-beta (TGF-β1) pathway, and vascularization substantially contribute to tumor aggressiveness.
Specifically, we found that secreted FMOD as an important regulator of glioma cell migration downstream of TGF-β1 pathway and forms a potential basis for therapeutic intervention in GBM.
We also found that vasculogenic mimicry was inhibited by galunisertib, a promising TGF-β1 inhibitor currently being studied in an ongoing trial in glioma patients.
The cell numbers of C6 glioma through Transwell chambers were decreased significantly (p < 0.01), and the expression of TGF-β1 was downregulated significantly (p < 0.01).
We present a positive correlation between the autocrine expression of YY1 and TGF-beta 1, IGF-1 and FGF-2, known to be involved in the progression of gliomas and meningiomas.
We present a positive correlation between the autocrine expression of YY1 and TGF-beta 1, IGF-1 and FGF-2, known to be involved in the progression of gliomas and meningiomas.
Unsupervised and supervised classification using the TGFbeta-responsive gene list in two independent glial tumor gene expression data sets revealed various levels of TGFbeta activation in these tumors.
This study was designed to evaluate if TGF-beta1 induces the expression and deposition of Tenascin-C in the extracellular matrix of high-grade gliomas which may be pivotal for the invasion of these tumors into healthy parenchyma.
RNA interference targeting TGF-beta1,2 results in a glioma cell phenotype that is more sensitive to immune cell lysis and less motile in vitro and nontumorigenic in nude mice, strongly confirming TGF-beta antagonism as a major therapeutic strategy for the future treatment of malignant gliomas.
Transforming growth factor-beta(1) (TGF-beta(1)) potently stimulates glioma cell motility whereas TGF-beta(2) is known for its immunosuppressive properties.
The results suggest that a complex balance between several components in the TGF-beta signalling pathway controls glioma responsiveness to TGF-beta1, and extend reports indicating that distinct signal transduction pathways are involved in growth inhibition and other cellular responses.
Analyses of TGF-beta receptors by means of affinity labeling in which 125I-TGF-beta1 was used showed that six glioma lines had both TGF-beta Types I and II receptors on their cell surfaces, whereas two lines had very small amounts of TGF-beta Type I and/or Type II receptors.