|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
High expression of cMyc and activation of the ERK1/2 pathway conferred resistance against alectinib in ALK expressing glioblastoma cells.
|
31776900 |
2020 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Interestingly, the inhibitory effect of TRIM48 overexpression on human GBM cell growth and the inactivation of ERK1/2 were significantly alleviated with additional curcumin treatment, while it the promoted the effect of siTRIM48 on human GBM cell growth, and the activation of ERK1/2 was significantly alleviated with additional PD98059 treatment.
|
31703057 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Moreover, the CXCL12-ERK1/2 signaling induces the expression of Ajuba, the main cofactor of AurA, which allows the auto-phosphorylation of AurA.We show that AurA contributes to glioblastoma cell survival, radio-resistance, self-renewal, and proliferation regardless of the exogenous stimulation with CXCL12.
|
30082913 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Providing a rationale for reports demonstrating miR-124-induced abrogation of GBM aggressiveness, we conclude that reversal of an ERK1/2-miR-124-SOX9 axis induces a neuronal phenotype and that enforcing neuronal differentiation represents a therapeutic strategy to improve outcomes in GBM.
|
31433983 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These findings highlight some potentially important particularities of the immune microenvironment in GBM and could provide an explanation for the recent observation that GBM with activated ERK1/2 signaling may respond better to anti-PD1 therapeutics.
|
31467175 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
These findings demonstrate a previously unknown feature ofSTAT3-mediated ERK1/2 regulation and an effective combination of two targets in resensitizing GBM to RT.
|
30986607 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Sulforaphane-cysteine induces apoptosis by sustained activation of ERK1/2 and caspase 3 in human glioblastoma U373MG and U87MG cells.
|
28393231 |
2017 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Knockdown of NUPR1 suppressed glioblastoma cell growth by arresting the cell cycle and inducing cell apoptosis via decreases in the expression of ERK1/2, p38 MAPK and caspase-3.
|
28000106 |
2017 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we provide a comprehensive overview on the functions of ERK1/2 in GBM and a rationale for treatment of GBM with ERK inhibitors.
|
28922853 |
2017 |
|
Glioblastoma Multiforme
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
We also demonstrated that ARRB1 mediated prolonged phosphorylation of ERK1/2 and Akt in glioblastoma cells induced by NK1R activation.
|
28341744 |
2017 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Results together suggest that the modulation of Stat3, CyclinB1, Alk, ezrin, merlin, and Erk1/2 functions contributes to the antitumor effects of 15α-MP against glioblastoma and breast cancer progression.<i></i>.
|
28069875 |
2017 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We emphasized three main aspects of signaling mechanisms induced by CBD treatment (alone or in combination with γ-irradiation) in human GBM that govern cell death: 1) CBD significantly upregulated the active (phosphorylated) JNK1/2 and MAPK p38 levels with the subsequent downregulation of the active phospho-ERK1/2 and phospho-AKT1 levels.
|
29088769 |
2017 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Whereas the ERK1/2 and STAT3 pathways independently promote proliferation and resistance to EGFR and c-MET co-inhibition, SHP2-driven ERK1/2 activity is dominant in driving cellular proliferation and SHP2-mediated antagonism of STAT3 phosphorylation prevails in the promotion of GBM cell death in response to EGFR and c-MET co-inhibition.
|
24951116 |
2014 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, these results suggested that GMFβ-dependent inactivation of the ERK1/2-Bcl-2/survivin pathway mediated the antiproliferative effect of β-elemene on glioblastoma.
|
24866280 |
2014 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, PI3K/Akt and ERK 1/2 signaling may be a target for adjuvant treatment of glioblastoma with a possible impact on tumor proliferation.
|
25056222 |
2014 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
These findings demonstrated that hCGβ phosphorylated ERK1/2 upregulating MMP-2 expression and activity leading to cell migration and invasion, suggesting that hCGβ, ERK1/2 and MMP-2 are the potential targets to inhibit glioblastoma invasion.
|
23232806 |
2013 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Phosphorylation of downstream ERBB signaling components (AKT, ERK1/2) and GBM CSC proliferation were inhibited by lapatinib.
|
22745588 |
2012 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In addition, levels of alpha-catenin S641 phosphorylation correlate with levels of ERK1/2 activity in human glioblastoma specimens and with grades of glioma malignancy.
|
19941816 |
2009 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results suggest that the activation of ERK1/2 is implicated in the pathobiology of glioblastoma.
|
18410277 |
2008 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In the present study, we demonstrate that CXC chemokine receptor 4 (CXCR4) is expressed in human glioblastoma U251 cell line, and that SDF-1 alpha increases the proliferation, chemotaxis, and invasion in CXCR4+ glioblastoma U251 cells through the activation of ERK1/2 and Akt.
|
17549698 |
2008 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Consistent with a role for SPR in cell growth, activation of SPR in U373 MG human glioblastoma cells leads to the phosphorylation of mitogen-activated protein kinases [extracellular signal-regulated kinase 1 and 2 (ERK1/2)] and stimulation of cell proliferation.
|
16012865 |
2005 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this study, we examined the role of ERK-1 in the regulation of MMP-9 production and the invasive behavior of the human glioblastoma cell line SNB19, in which ERK1 is constitutively activated.
|
12165859 |
2002 |
|
Glioblastoma Multiforme
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We further studied the activation and inhibition of uPA promoter by co-expression of a transactivation domain lacking c-jun: a dominant negative ERK1 and ERK2 mutant and a dominant negative c-raf in glioblastoma cell line showed repressed uPA promoter activity compared with the effect of the empty expression vector.
|
11115541 |
2001 |
|
Glioblastoma Multiforme
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We further studied the inhibition of uPAR promoter by coexpression of a transactivation domain lacking C-Jun; a dominant-negative ERK1 and ERK2 mutant and a dominant-negative C-raf in glioblastoma cell lines showed the repressed uPAR promoter activity compared with the effect of the empty expression vector.
|
11234878 |
2001 |