Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
<i>NEAT1</i> depletion also inhibited GBM cell growth and invasion in the intracranial animal model.<b>Conclusions:</b> The EGFR/<i>NEAT1</i>/EZH2/β-catenin axis serves as a critical effector of tumorigenesis and progression, suggesting new therapeutic directions in glioblastoma.<i></i>.
|
29138341 |
2018 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
A Novel Positive Feedback Loop Between NTSR1 and Wnt/β-Catenin Contributes to Tumor Growth of Glioblastoma.
|
29065410 |
2017 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Aberrant activation of beta-catenin/TCF4 and STAT3 signaling in glioblastoma multiforme (GBM) has been reported.
|
23295773 |
2013 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Additionally, tunicamycin increased the expression of maternally expressed gene-3 (MEG-3) and wingless/integrated (Wnt)/β-catenin in glioblastoma cells.
|
30127865 |
2018 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Additionally, we show that the degradation of another β-TrCP1 substrate, β-catenin, is impaired and accumulates in the cytosol of glioblastoma cell lines.
|
21454620 |
2011 |
Glioblastoma Multiforme
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Among these are two compounds, ICG-001, targeting CREB binding protein (CREBBP), and PKF118-310, targeting β-catenin (CTNNB1), which have not been tested previously for effectiveness against GBM.
|
23408876 |
2013 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Bcl-w promotes the mesenchymal traits of glioblastoma cells by inducing vimentin expression via activation of transcription factors, β-catenin, Twist1 and Snail in glioblastoma U251 cells.
|
23826359 |
2013 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Casein kinase 2α regulates glioblastoma brain tumor-initiating cell growth through the β-catenin pathway.
|
25241897 |
2015 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Epigenetic silencing of miR-338 facilitates glioblastoma progression by de-repressing the pyruvate kinase M2-β-catenin axis.
|
28858851 |
2017 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Here, we identified that β-catenin mRNA and protein levels were up-regulated in GBM tissues and four kinds of glioblastoma cell lines, including T98G, A172, U87, and U251 cells, compared with normal brain tissue and astrocytes.
|
28615958 |
2017 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
However, the mechanisms of down-regulation of β-catenin that represses glioblastoma malignancy behavior remain to be elucidated.
|
20969832 |
2010 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In 74 gliomas of different histological grade and in 24 glioblastoma cell lines, protein expression of WNT member 3a (WNT3a), β-catenin and transcription factor 4 (TCF4) was investigated by immunohistochemistry, western blotting, immunofluorescence and immunocytochemistry.
|
26708597 |
2016 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, miR-370 inhibited the proliferation of human glioma cells by regulating the levels of β-catenin and the activation of FOXO3a, suggesting that miR-370 was a tumor suppressor in the progression of human astrocytoma and glioblastoma cells.
|
29399110 |
2018 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
In fact, besides being a well-known downstream event of mTOR hyper-activation, autophagy downregulation is also bound to the effects of aberrantly activated Notch, Hedgehog, and Wnt/β-catenin pathways in GBM.
|
31387280 |
2019 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In terms of mechanism, we found that SNHG7 directly inhibited miR-5095, which targeted the 3' UTR of CTNNB1 mRNA and subsequently downregulated the Wnt/β-catenin signaling pathway in GBM.
|
29360452 |
2018 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Inhibiting TCF, or silencing TCF4 or CTNNB1/β-catenin upregulated SQSTM1/p62 in GBM at transcriptional and protein levels and, in turn, autophagy.
|
29313411 |
2018 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Inhibition of Bevacizumab-induced Epithelial-Mesenchymal Transition by BATF2 Overexpression Involves the Suppression of Wnt/β-Catenin Signaling in Glioblastoma Cells.
|
28739720 |
2017 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Methylation-mediated silencing of microRNA-211 promotes cell growth and epithelial to mesenchymal transition through activation of the AKT/β-catenin pathway in GBM.
|
28445937 |
2017 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
MSX1 inhibits cell migration and invasion through regulating the Wnt/β-catenin pathway in glioblastoma.
|
26271668 |
2016 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
NF-kappaB positively regulated beta-catenin/Tcf pathways in human glioblastoma, whereas it has an opposite effect on beta-catenin/Tcf pathways in colon, liver, and breast cancer cells.
|
18242184 |
2008 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data indicate, for the first time, that autophagy induction results in Wnt signalling attenuation and in β-catenin relocalisation within the GBM cell.
|
30442596 |
2019 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results revealed that β-catenin and miR-21 were concordantly expressed in GBM cell lines, and SFN significantly reduced miR-21 expression through inhibiting the Wnt/β-catenin/TCF4 pathway.
|
25991372 |
2015 |
Glioblastoma Multiforme
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Recent reports describe BRAF<sup>V600E</sup> mutation in malignant peripheral nerve sheath tumors, and aberrant Wnt signaling and CTNNB1 (β-catenin gene) mutations have been described in GBM.
|
26932501 |
2016 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
SIGNIFICANCE: These findings identify the β-catenin-USP1-EZH2 signaling axis as a critical mechanism for glioma tumorigenesis that may serve as a new therapeutic target in glioblastoma.
|
30425057 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Subsequent genetic inhibition experiments showed that suppression of MACF1 selectively inhibited glioblastoma cell proliferation and migration in cell lines established from patient derived xenograft mouse models and immortalized glioblastoma cell lines that were associated with downregulation of the Wnt-signaling mediators, Axin1 and β-catenin.
|
27959385 |
2017 |