|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
LASP1 may function as an oncogene in GBM and regulate cell proliferation and chemosensitivity in a PI3K/AKT-dependent mechanism.
|
29980193 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Resveratrol targeting of AKT and p53 in glioblastoma and glioblastoma stem-like cells to suppress growth and infiltration.
|
27419830 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, to date, all the attempts to target this pathway with PI3K, AKT, or mTORC1 inhibitors failed to improve the outcome of patients with GBM.
|
30662577 |
2018 |
|
Glioblastoma
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Another finding showed that flavopiridol treatment induced a substantial AKT-Ser473 phosphorylation in human glioblastoma T98G cell line in contrast to siRNA-mediated inhibition of Cdk9 and Cdk9 combined with Cdk7, whereas siRNA-mediated silencing of Cdk7 caused a minor increase in AKT-Ser473 phosphorylation.
|
22391209 |
2012 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this review we focus on the function of AKT/GSK3β signaling in GBM.
|
27568206 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
For example, combining gefitinib with inhibitors of the PI3K/AKT pathway show enhanced cytotoxicity in glioblastoma derived cell lines.
|
18566746 |
2008 |
|
Glioblastoma
|
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
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
SiRNA knockdown of KIF14 inhibited tumor growth in vitro and in vivo, attenuated anchorage-independent growth, and induced G2/M phase arrest, cytokinesis failure and apoptosis in glioblastoma cell lines in association with decreased AKT phosphorylation and activity.
|
26536004 |
2015 |
|
Glioblastoma
|
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
|
0.100 |
Biomarker
|
disease |
BEFREE |
Though the molecular mechanisms of protein kinase B (AKT) survival signal have been comprehensively explored, the role of miR-149 in glioblastoma (GBM) and its regulation on AKT signaling have not yet been ascertained.
|
23298478 |
2013 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results suggest that activation of the InsR/IGF1R pathway confers resistance to EGFR inhibitors in EGFR-dependent glioblastoma through AKT regulation.
|
26561558 |
2016 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
MicroRNA-149 is epigenetically silenced tumor-suppressive microRNA, involved in cell proliferation and downregulation of AKT1 and cyclin D1 in human glioblastoma multiforme.
|
27783537 |
2016 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Enforced expression of PAK4 rescued miR‑485 tumour‑suppressor functions in GBM cells. miR‑485 inhibited the activation of the AKT and ERK signalling pathways in GBM.
|
29048626 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Up-regulated circular RNA hsa_circ_0067934 contributes to glioblastoma progression through activating PI3K-AKT pathway.
|
31081099 |
2019 |
|
Glioblastoma
|
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
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
HBP1 phosphorylation by AKT regulates its transcriptional activity and glioblastoma cell proliferation.
|
29355710 |
2018 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We also demonstrate that activated AKT is strongly correlated with elevated Ser(P)(199)-hnRNP A1 levels in a panel of 22 glioblastomas.
|
21454539 |
2011 |
|
Glioblastoma
|
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
|
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 |
Synemin promotes AKT-dependent glioblastoma cell proliferation by antagonizing PP2A.
|
22337773 |
2012 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Perifosine enhances bevacizumab-induced apoptosis and therapeutic efficacy by targeting PI3K/AKT pathway in a glioblastoma heterotopic model.
|
28616662 |
2017 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our data provides evidence that JNK2alpha2 is the major active JNK isoform and is involved in the promotion of proliferation and growth of human glioblastoma tumors through specific activation of AKT and overexpression of eIF4E.
|
17047065 |
2006 |
|
Glioblastoma
|
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
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, due to the development of resistance mechanisms, kinase inhibition studies targeting the PI3K-AKT pathway for relapsing glioblastoma have mostly failed thus far.
|
25256166 |
2014 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, SDF-1-CXCR4 pathway induced the expression of AGR2 to control the progression of EMT likely via AKT pathway in the development of glioblastoma.
|
26608373 |
2016 |