|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We found that the combination of TP4 and p38 inhibitors (SB202190 and VX-745) enhanced cytotoxicity in U251 glioblastoma cells but not noncancerous neural cells.
|
31673920 |
2020 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In summary, we have discovered hesperetin as a natural product candidate for the treatment of GBM, and that it could induce GBM cell apoptosis via p38 MAPK activation.
|
31295040 |
2020 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
cMyc and ERK activity are associated with resistance to ALK inhibitory treatment in glioblastoma.
|
31776900 |
2020 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Rescue experiments confirm that TIPE3 inhibits GBM cell apoptosis via the p38 MAPK pathway.
|
30639532 |
2019 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We found that knockdown of LKB1 significantly promoted <i>in vitro</i> proliferation, adhesion, invasion, and metformin-induced apoptosis, and simultaneously enhanced activation of ERK and mammalian-target of rapamycin (mTOR) signaling pathways in LKB1-compenent U87 and T98 glioblastoma cells.
|
31497348 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We will therefore shortly embark on a clinical trial of adoptively transferred, p38 MAPK-inhibited cDC2 in adults with GBM.
|
31143512 |
2019 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Moreover, TP4 induced mitochondrial hyperpolarization and dysfunction, which preceded the elevation of intracellular reactive oxygen species, DNA damage, and necrotic cell death in both U87MG and U251 glioblastoma cells. p38 was also activated by TP4, but did not contribute to cytotoxicity.
|
30717309 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Deletion of the ERK binding site resulted in stabilization of CIC and increased therapeutic efficacy of ERK inhibition in GBM models.
|
30737375 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Ultrasound enhanced anti-tumor effect of temozolomide in glioblastoma cells <i>via</i> JNK and p38 pathways.
|
31719901 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
PRL-3 is a potential glioblastoma prognostic marker and promotes glioblastoma progression by enhancing MMP7 through the ERK and JNK pathways.
|
29556339 |
2018 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results show that chrysin exerts anticancer activity in glioblastoma cell lines possibly via the ERK/Nrf2 signaling pathway and indicate the potential application of chrysin as a natural sensitizer in chemotherapy.
|
29662304 |
2018 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
C-27-carboxylated oleanane triterpenoids up-regulate TRAIL DISC assembly via p38 MAPK and CHOP-mediated DR5 expression in human glioblastoma cells.
|
30359578 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, our data identified MAPK-ERK-YAP signaling pathways as the primary molecular mechanisms by which TNFα modulated mitochondrial fission and glioblastoma apoptosis.
|
30425514 |
2018 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
This is a desired feature for intracellular drug delivery, since the endocytic pathway otherwise transfers the drugs into lysosomes where they can be degraded without reaching their intended target. siRNA-transfection was successful in C6 and U87 cell lines using the G3 and G4 dendrimers followed by a decrease of approximately 20% of target protein p42-MAPK expression.
|
30110914 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Knockdown of EPHA2 and EPHA3 together led to increased expression of differentiation marker GFAP and blocked clonogenic and tumorigenic potential, promoting significantly higher survival <i>in vivo</i> Treatment of rGBM with a bispecific antibody against EPHA2/A3 reduced clonogenicity <i>in vitro</i> and tumorigenic potential of xenografted recurrent GBM <i>in vivo</i> via downregulation of AKT and ERK and increased cellular differentiation.
|
29945963 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These novel outcomes suggested that knockdown of HDAC1 possibly suppressed the expression of phosphorylated AKT (p-AKT) and phosphorylated ERK (p-ERK) proteins, while overexpression of HDAC1 significantly increased p-AKT and p-ERK protein in glioblastoma cells.
|
29782850 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Targeting the interaction between the carboxy terminus of Cx43 and Akt/ERK could be an effective therapeutic strategy against GBM.
|
29931708 |
2018 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These data suggest that when overexpressed, EphA2 induces ERK activation through its tyrosine kinase activity, leading to S897 phosphorylation and promotion of glioblastoma cell proliferation.
|
29626472 |
2018 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Increased expression and activity of p38 MAPK is correlated with poor prognosis in cancer, including glioblastoma multiforme; however, the toxicity of p38 MAPK inhibitors limits their clinical use.
|
29316898 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Mutual Stabilization between TRIM9 Short Isoform and MKK6 Potentiates p38 Signaling to Synergistically Suppress Glioblastoma Progression.
|
29669288 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Knockdown of arsenic resistance protein 2 inhibits human glioblastoma cell proliferation through the MAPK/ERK pathway.
|
30542699 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
miR-129-5p targets Wnt5a to block PKC/ERK/NF-κB and JNK pathways in glioblastoma.
|
29531296 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Metabolic Reprogramming by Dual AKT/ERK Inhibition through Imipridones Elicits Unique Vulnerabilities in Glioblastoma.
|
30037819 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Interaction network analysis indicated that the GBM-associated proteins in the RNA processing were linked to crucial signaling transduction modulators including epidermal growth factor receptor (EGFR), signal transducer and activator of transcription 1 (STAT1), and mitogen-activated protein kinase 1 (MAPK1), which were further connected to the proteins important for neuronal structural integrity, development and functions.
|
28341197 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
A Rationale for Targeting Extracellular Regulated Kinases ERK1 and ERK2 in Glioblastoma.
|
28922853 |
2017 |