Glioblastoma Multiforme
|
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 Multiforme
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Moreover, we demonstrate the existence of a positive correlation between the expression levels of HIF-1α, TCF1 and neuronal phenotype in GBM tumors, accompanied by the over-expression of several Wnt signaling components, finally affecting patient prognosis.
|
31410187 |
2019 |
Glioblastoma Multiforme
|
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 Multiforme
|
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 Multiforme
|
0.400 |
Biomarker
|
disease |
BEFREE |
Hypermethylated gene ANKDD1A is a candidate tumor suppressor that interacts with FIH1 and decreases HIF1α stability to inhibit cell autophagy in the glioblastoma multiforme hypoxia microenvironment.
|
30082910 |
2019 |
Glioblastoma Multiforme
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Expression of HIF-1α was measured as a potential target gene of miR-448 in glycolysis.RESULTSmiR-448 was detected and determined to be significantly downregulated in both glioma tissues from glioma patients and GBM cell lines.
|
31003211 |
2019 |
Glioblastoma Multiforme
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The present study therefore aimed to examine the expression levels of HIF-1α and CAV1, and their association with GBM prognosis.
|
30854062 |
2019 |
Glioblastoma Multiforme
|
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 Multiforme
|
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 Multiforme
|
0.400 |
Biomarker
|
disease |
BEFREE |
By promoting the adaptation to non-adherent conditions, mechanisms driven by HIF-1α may considerably contribute to the biology and aggressiveness of glioblastoma.
|
31128911 |
2019 |
Glioblastoma Multiforme
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Therefore, our findings uncover a hypoxia-induced negative feedback mechanism that maintains high activity of HIF-1 and cell mobility in human glioblastoma.
|
29860315 |
2018 |
Glioblastoma Multiforme
|
0.400 |
Biomarker
|
disease |
BEFREE |
We also found that HIF-2α downregulation sensitized the GBM cells to cisplatin to a greater extent than HIF-1α, whereas CD133 knockdown had a more marked effect on cisplatin sensitisation than knockdown of either one of the HIFs, suggesting the existence of a HIF-independent cisplatin resistance mechanism mediated by CD133.
|
29492900 |
2018 |
Glioblastoma Multiforme
|
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 Multiforme
|
0.400 |
Biomarker
|
disease |
BEFREE |
These findings provide a new link in the mechanistic understanding of TMZ resistance under glioma hypoxia microenvironment, and consequently HIF-1α/miR-26a/Bax/Bad signaling pathway as a promising adjuvant therapy for GBM with TMZ.
|
30425242 |
2018 |
Glioblastoma Multiforme
|
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 Multiforme
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Clinical positron emission tomography studies using radiolabeled Cu-ATSM have shown that Cu-ATSM accumulates in glioblastoma and its uptake is associated with high hypoxia-inducible factor-1α expression.
|
29154146 |
2018 |
Glioblastoma Multiforme
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Through bioinformatics analysis, the high expression of HIF-1α, MCT1 or MCT4 indicate a poor prognosis in glioblastoma.
|
29928884 |
2018 |
Glioblastoma Multiforme
|
0.400 |
Biomarker
|
disease |
BEFREE |
CCL20 was secreted in a hypoxia-dependent manner from astrocytes and busted the hypoxic induction of HIF-1α in glioblastoma cells.
|
29535421 |
2018 |
Glioblastoma Multiforme
|
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 Multiforme
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
While HIF1α has been widely studied in cancer, HIF2α offers a potentially more specific and appealing target in glioblastoma given expression in glioma stem cells and not normal neural progenitors, activation in states of chronic hypoxia and expression that correlates with glioma patient survival.
|
30089425 |
2018 |
Glioblastoma Multiforme
|
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 Multiforme
|
0.400 |
Biomarker
|
disease |
BEFREE |
Hypoxia-Inducible Factor-1α Activity as a Switch for Glioblastoma Responsiveness to Temozolomide.
|
30013951 |
2018 |
Glioblastoma Multiforme
|
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 Multiforme
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, the liposomes made better modulation of glioblastoma microenvironment such as the down-regulation of CD31-positive tumor vessels and HIF-1α expression.
|
28252970 |
2017 |
Glioblastoma Multiforme
|
0.400 |
Biomarker
|
disease |
BEFREE |
The present review focuses on the strategies through which to target HIF-1α and the related downstream genes highlighting their regulatory roles in angiogenesis, apoptosis, migration and glucose metabolism for the development of future GBM therapeutics.
|
27959421 |
2017 |