Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
A CD133-AKT-Wnt signaling axis drives glioblastoma brain tumor-initiating cells.
|
31695152 |
2020 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data indicate that the impaired circRNA expression of the AKT3 gene contributes to GBM tumorigenesis, and our data corroborate the hypothesis that restoring AKT3-174aa while inhibiting activated AKT may provide more benefits for certain GBM patients.
|
31470874 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
<b>Abbreviations</b>: AKT1: AKT serine/threonine kinase 1; ATG14: autophagy related 14; BECN1: Beclin 1; DDR1: discoidin domain receptor tyrosine kinase 1; ECM: extracellular matrix; GBM: glioblastoma multiforme; MTOR: mechanistic target of rapamycin kinase; PDGFR: platelet derived growth factor receptor; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; RPTOR: regulatory associated protein of MTOR complex 1; RICTOR: RPTOR independent companion of MTOR complex 2.
|
31117874 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, DPT effectively inhibited the expression of PI3K and downregulated PI3K/Akt‑mediated signaling pathways to prevent glioblastoma progression.
|
30816477 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Oncogenic Ras is downregulated by ARHI and induces autophagy by Ras/AKT/mTOR pathway in glioblastoma.
|
31088402 |
2019 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These data justify to explore combined targeted therapy approaches in glioblastoma that aim at down-regulating AKT function to enhance the therapeutic potential of dual PI3K/mTOR inhibitors.
|
31618458 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
The PI3K/AKT/mTOR pathway activation plays a central role in glioblastoma multiforme (GBM) development and progression, and in resistance to anti-cancer therapies.
|
31707687 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
2-(2-(2,4-dioxopentan-3-ylidene)hydrazineyl)benzonitrile as novel inhibitor of receptor tyrosine kinase and PI3K/AKT/mTOR signaling pathway in glioblastoma.
|
30731398 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
ARL4C stabilized by AKT/mTOR pathway promotes the invasion of PTEN-deficient primary human glioblastoma.
|
30357833 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Interaction of Discoidin Domain Receptor 1 with a 14-3-3-Beclin-1-Akt1 Complex Modulates Glioblastoma Therapy Sensitivity.
|
30917320 |
2019 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Notch activity in GBM was also shown to be associated with hypoxia and certain cancer-related molecular pathways such as PI3K/AKT/mTOR and ERK/MAPK.
|
31376551 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Specifically, targeting cellular pathways frequently altered in glioblastoma, such as the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR), the p53 and the retinoblastoma (RB) pathways, or epidermal growth factor receptor (EGFR) gene amplification or mutation, have failed to improve outcome, likely because of redundant compensatory mechanisms, insufficient target coverage related in part to the blood brain barrier, or poor tolerability and safety.
|
31541850 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Up-regulated circular RNA hsa_circ_0067934 contributes to glioblastoma progression through activating PI3K-AKT pathway.
|
31081099 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, the present study demonstrated that TIGAR may promote glioblastoma growth and progression through oxidation resistance and AKT activation.
|
31402948 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
MicroRNA-562 negatively regulated c-MET/AKT pathway in the growth of glioblastoma cells.
|
30613151 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
It inhibits signaling through the PI3/AKT axis and other cascades of biologic importance in glioblastoma, and has promising pre-clinical activity in vitro and in vivo.
|
31325145 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
We conclude that BAS-4 showed potential activity against glioma by inducing apoptosis mediated by ΔΨm loss and AKT pathway disruption, and future studies should further evaluate BAS-4 as a promising antineoplastic agent against glioblastoma.
|
30856536 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings suggest that patient-derived glioblastoma stem cells in the context of ERK and AKT activation are sensitive and highly regulated by neddylation inhibition.
|
31771104 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
The RNA‑seq analysis revealed that the PI3K‑AKT pathway played an important role in GBM.
|
31485609 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
The effect of miR-579 on the PI3K/AKT pathway in human glioblastoma PTEN mutant cell lines.
|
31243804 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Nevertheless, the administration of the dual PI3K/mTOR inhibitor BEZ235 potentiated the effect of TMZ plus MET on cell viability, inducing a pro-apoptotic phenotype during hypoxic condition also in T98 cells, suggesting the block of the PI3K/AKT/mTOR pathway as a complementary target to further overcome GBM resistance during hypoxia.
|
31214505 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
The present study also demonstrated that vitexin inhibited RAC‑alpha serine/threonine‑protein kinase (Akt)/mechanistic target of rapamycin kinase (mTOR) signaling in human glioblastoma cells.
|
29328424 |
2018 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
In summary, Evo inhibits cell proliferation by inducing cellular apoptosis via suppressing PI3K/AKT and activating MAPK in GBM; these results indicate that Evo may be regarded as a new approach for GBM treatment.
|
29535541 |
2018 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therapies targeting the PI3K/AKT/Afadin pathway may therefore be beneficial for reducing the angiogenic potential of glioblastoma.
|
29434887 |
2018 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
HBP1 phosphorylation by AKT regulates its transcriptional activity and glioblastoma cell proliferation.
|
29355710 |
2018 |