|
Glioblastoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The expression levels of LOX, BMP1 and HIF1A were correlated and analyzed according to IDH1 mutation status and to the clinical end-point of overall survival of glioblastoma patients.
|
25790191 |
2015 |
|
Glioblastoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The findings of the current study demonstrate presence of the IDH1 R132H mutation in primary human glioblastoma cell lines with upregulated HIF-1α expression, downregulating c-MYC activity and resulting in a consequential decrease in miR-20a, which is responsible for cell proliferation and resistance to standard temozolomide treatment.
|
29625108 |
2018 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Moreover, miR-215 expression correlates inversely with KDM1B while correlating positively with HIF1α and GBM progression in patients.
|
26766590 |
2016 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our findings elucidate a mechanism whereby LSD1 controls senescence in Glioblastoma tumor cells through the regulation of HIF-1α, and we propose the novel defined LSD1/HIF-1α axis as a new target for the therapy of Glioblastoma tumors.
|
30951900 |
2019 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Taken together, our data suggest that KDELR2 is a target gene downstream of HIF1-alpha driving the malignancy of GBM and could eventually serve as a therapeutic target for the treatment of GBM patients.
|
31342232 |
2019 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
The aforementioned results demonstrate that hypoxia could induce enhancements of migration and invasion by activating PI3K/Akt/mTOR pathway by targeting HIF-1α in human glioblastoma U87 cells, which provide a theoretical basis for the treatments of GBM by targeting the PI3K/Akt/mTOR/HIF-1α pathway.
|
30371540 |
2018 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Epileptogenic GBMs correlate with decreased hypoxia/ HIF-1α/STAT5b signaling compared to glioblastomas that do not present with epilepsy.
|
30621209 |
2019 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
The expression of FAT1, EMT (Snail/LOX/Vimentin/N-cad), stemness (SOX2/OCT4/Nestin/REST) and hypoxia markers (HIF-1α/VEGF/PGK1/CA9) was upregulated in ≥39% of GBM tumors (n = 31) with significant positive correlation (p ≤ 0.05) of the expression of FAT1 with LOX/Vimentin/SOX2/HIF-1α/PGK1/VEGF/CA9.
|
28994107 |
2018 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Anoxia induces macrophage inhibitory cytokine-1 (MIC-1) in glioblastoma cells independently of p53 and HIF-1.
|
12082608 |
2002 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
These findings therefore suggest that N-myc/Sox4-mediated ALK signaling cascades containing Stat3, Akt, HIF-1α, and VEGF-A confer multiple advantages to tumor growth through alterations in neovascularization and cell proliferation in GBMs.
|
28837676 |
2017 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Suppression of hypoxia-inducible factor 1α (HIF-1α) has been shown to sensitize glioblastoma cells to temozolomide (TMZ) treatment via down-modulation of O6-methylguanine-DNA methyltransferase (MGMT) expression.
|
23970362 |
2013 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
CTD_human |
Geldanamycin inhibits migration of glioma cells in vitro: a potential role for hypoxia-inducible factor (HIF-1alpha) in glioma cell invasion.
|
12811834 |
2003 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
FGFR1 Induces Glioblastoma Radioresistance through the PLCγ/Hif1α Pathway.
|
26896280 |
2016 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Taken together, these results suggest that DT at clinically achievable concentration functions as an inhibitor of HIF-1α, worthy of further investigations in the therapy of glioblastoma.
|
28410215 |
2017 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
In brief, for the first time, these results reveal an upstream master regulatory role of FAT1 in the expression and role of HIF1α under hypoxic conditions and that FAT1-HIF1α axis controls the invasiveness of GBM.
|
27536856 |
2016 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Hypoxia plays important roles in the prognosis of malignant brain tumors such as glioblastoma because it causes drug delivery deficiencies and the induction of hypoxia-inducible factor-1α in tumor cells.
|
31252311 |
2019 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
PTEN status mediates 2ME2 anti-tumor efficacy in preclinical glioblastoma models: role of HIF1α suppression.
|
24162827 |
2014 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
HIF-1α Is a Metabolic Switch between Glycolytic-Driven Migration and Oxidative Phosphorylation-Driven Immunosuppression of Tregs in Glioblastoma.
|
30943404 |
2019 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
The HIF‑1α/miR‑224‑3p/ATG5 axis affects cell mobility and chemosensitivity by regulating hypoxia‑induced protective autophagy in glioblastoma and astrocytoma.
|
30569180 |
2019 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Advances in the targeting of HIF-1α and future therapeutic strategies for glioblastoma multiforme (Review).
|
27959421 |
2017 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Here, we review the roles of HIF-1α and AHR in cancer and immune cell metabolism in GBM.
|
28318896 |
2017 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Restoration of wild-type PTEN to glioblastoma cell lines lacking functional PTEN ablates hypoxia and IGF-1 induction of HIF-1-regulated genes.
|
10691731 |
2000 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Intriguingly, the GBM sub-population enriched of cancer stem cells (CD133(+) fraction) is the primary target of the pro-differentiating effects mediated by the crosstalk between HIF-1α, Wnt, and Notch signalling.
|
23429286 |
2013 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our data reported that ASA affected GBM-EC viability, tube-like structure formation, cell migration, and VEGF releasing in a dose-dependent manner and that combined treatments with TMZ, BEV, and SUN synergized to counteract proangiogenic cell ability. mRNA expression analysis displayed a marked effect of ASA in reducing VEGF, VEGFR-1, HIF-1α, RAS, mitogen-activated protein kinase kinase, AKT, and BCL-2, as well a combined anticancer effect of ASA together with TMZ, BEV, and SUN.
|
30144594 |
2018 |
|
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Focusing on inhibiting the signaling pathways, which are associated with hypoxia-mediated maintenance of glioblastoma stem cells or the knockdown of the hypoxia-inducible factor 1-alpha (HIF1α), may help to the develop new target-specific treatments.
|
26559087 |
2015 |