|
Glioblastoma Multiforme
|
0.500 |
CausalMutation
|
disease |
CGI |
|
|
|
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Using two different migration assays, Western blotting, conventional and super-resolution (dSTORM) fluorescence microscopy we examine the effects of the dual PI3K/mTOR-inhibitor PI-103 alone and in combination with the Hsp90 inhibitor NVP-AUY922 and/or irradiation on the migration, expression of marker proteins, focal adhesions and F-actin cytoskeleton in two GBM cell lines (DK-MG and SNB19) markedly differing in their invasive capacity.
|
28424411 |
2017 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
We have examined the relative roles of the two major phospholipid products of PI3K activity, phosphatidylinositol 3,4-biphosphate [PtdIns(3,4)P2] and phosphatidylinositol 3,4,5-triphosphate [PtdIns(3,4,5)P3], in the regulation of PKB activity in glioblastoma cells containing high levels of both of these lipids due to defective PTEN expression.
|
10958682 |
2000 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
The PI3K/AKT/mTOR pathway is commonly over activated in glioblastoma (GBM), and Rictor was shown to be an important regulator downstream of this pathway.
|
23555046 |
2013 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, the current study demonstrated for the first time that inhibition of RWDD3 expression inhibited glioblastoma progression, at least partly, via suppressing the PI3K/AKT signaling activity, and thus RWDD3 may be a novel potential therapeutic target for glioblastoma.
|
29977365 |
2018 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
We previously developed a non-germline genetically engineered mouse model of GBM in which PI3K and MAPK are activated via Pten deletion and KrasG12D in immortalized astrocytes.
|
28379424 |
2017 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
This RTK/PTEN/PI3K pathway leads to activated AKT and phospho-AKT levels are elevated in the majority of GBM tumor samples and cell lines, which studies show help glioma cells grow uncontrolled, evade apoptosis, and enhance tumor invasion.
|
21827416 |
2011 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Rapamycin has anticancer activity in PTEN-deficient glioblastoma and warrants further clinical study alone or in combination with PI3K pathway inhibitors.
|
18215105 |
2008 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Therefore, while under normoxic conditions, EGF stimulates the activation of both the PI3K and the MAPK pathways and the induction of VEGF, in glioblastoma cells, hypoxic conditions lead to the suppression of the PI3K/RhoA/C pathway and an exclusive switch to the MAPK pathway.
|
31698752 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
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
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
TGF-β1 targets Smad, p38 MAPK, and PI3K/Akt signaling pathways to induce PFKFB3 gene expression and glycolysis in glioblastoma cells.
|
28834297 |
2017 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Further, photofrin based PDT followed by miR-99a transfection dramatically increased miR-99a expression and also increased apoptosis in glioblastoma cell cultures and drastically reduced tumor growth in athymic nude mice, due to down regulation of fibroblast growth factor receptor 3 (FGFR3) and PI3K/Akt signaling mechanisms leading to inhibition of cell proliferation and induction of molecular mechanisms of apoptosis.
|
23409016 |
2013 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Here we show that overexpression of NEU3 in glioblastoma U87MG cells activates PI3K/Akt signaling pathway resulting in an increased radioresistance capacity and in an improved efficiency of double strand DNA-repair mechanisms after irradiation.
|
30466783 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Both pathways are also activated in GBM cell lines, however, only the PI3K pathway seems to play a crucial role in resistance to alkylating agents and might serve as drug target for chemosensitization.
|
29755294 |
2018 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
GDC-0084 is a brain penetrant, dual PI3K/mTOR inhibitor that has shown promising activity in a preclinical model of glioblastoma.
|
30796030 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
The phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway is over-activated in glioblastoma and has been revealed to be potentially implicated in resistance to TMZ.
|
29151909 |
2017 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
We previously reported that decreased miR-218 expression in GBM directly promotes RTK activity by increasing the expression of key RTKs and their signaling mediators, including the RTK epidermal growth factor receptor (EGFR), phospholipase C-γ1 (PLCγ1), and the kinases PIK3CA and ARAF.
|
25943352 |
2015 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Insulin growth factor-2 binding protein 3 (IGF2BP3) is a glioblastoma-specific marker that activates phosphatidylinositol 3-kinase/mitogen-activated protein kinase (PI3K/MAPK) pathways by modulating IGF-2.
|
21613208 |
2011 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
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
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
PI3K-AKT pathway negatively controls EGFR-dependent DNA-binding activity of Stat3 in glioblastoma multiforme cells.
|
16007122 |
2005 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
PIK3R3, the gene that encodes the PI3K regulatory subunit p55γ, is over-expressed in glioblastoma and ovarian cancers, but its expression in gastric cancer (GC) is not known.
|
22876838 |
2012 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
The PI3K pathway is commonly activated in glioblastoma and promotes tumor cell survival, suggesting that its inhibition would make cells more sensitive to cytotoxic agents.
|
20473884 |
2011 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
The activation of PI3K/Akt1 signaling pathway is involved in the proliferation of glioblastoma; however, the underlying mechanism of Akt1 activation during the development of glioblastoma remains largely unclear.
|
25501279 |
2015 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Treatment of a panel of established GBM cell lines (U138MG, U87, U373 and C6) with pharmacological NFκB inhibitors (BAY117082, parthenolide, MG132, curcumin and arsenic trioxide) and NFκB-p65 siRNA markedly decreased the viability of GBMs as compared to inhibitors of other signaling pathways such as MAPKs (ERK, JNK and p38), PKC, EGFR and PI3K/Akt.
|
21040711 |
2011 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Taken together, these findings suggest that EGFR signaling activates downstream PI3K/Akt to increase MMP9 expression in glioblastoma, while phosphorylation of Akt is a control point by miRNA-181c.
|
24867100 |
2014 |