|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We analysed the transcript expression of CLEC5A in glioblastoma by accessing The Cancer Genome Atlas (TCGA). qRT-PCR was performed to detect the RNA expression of genes in cells and tissues, and Western blot was used to measure the protein levels (Cyclin D1, Bcl-2, BAX, PCNA, MMP2, MMP9, Akt and Akt phosphorylation) in tissues and cells.
|
30834619 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this study, we examined whether inhibition of the anti-apoptotic Bcl-2 family proteins Bcl-2 and Bcl-xL enhances the biological effects of the repurposed CUSP9 regimen in an in vitro setting of glioblastoma.
|
31222722 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Accumulating evidence indicates that resistance to apoptosis in GB is mediated via upregulation of pro-survival BCL2-family members.
|
30389373 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Treatment with a Bcl2 inhibitor does not fully explain the effect of gossypol on glioblastoma.
|
31658771 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therefore, we combined ITs (9.2.27-PE38KDEL or Mel-14-PE38KDEL) targeting chondroitin sulfate proteoglycan 4 (CSPG4) with a panel of Bcl-2 family inhibitors (ABT-737, ABT-263, ABT-199 [Venetoclax], A-1155463, and S63845) against patient-derived glioblastoma, melanoma, and breast cancer cells/cell lines.
|
30625226 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data indicate that concomitant inhibition of RAC1 and Bcl-2/Bcl-xL induces pro-apoptotic and anti-migratory glioblastoma phenotypes as well as synergistic anti-neoplastic activities.
|
30859392 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Elevated ZHX1 expression correlated with poor prognosis in GBM patients, and in vitro studies demonstrated that ZHX1 attenuated GBM cell apoptosis by downregulation of pro-apoptotic protein (Bax) and upregulation of anti-apoptotic protein (Bcl-2).
|
31648104 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Hence, this study collectively revealed that the increase in ROS level is at least one of the mechanisms associated with auraptene-induced GBM cell toxicity as well as the induction of apoptosis through Bax/Bcl-2 modulation and genes expression involved that contribute to the cytotoxicity of auraptene in U87 cells.
|
31611741 |
2019 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
CTRP8-induced RXFP1 activation caused an increase in cellular protein levels of the anti-apoptotic Bcl members and STAT3 targets Bcl-2 and Bcl-XL in human GBM.
|
29949238 |
2018 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, our findings demonstrate that KPNB1 is required for proteostasis maintenance and its inhibition induces apoptosis in glioblastoma cells through UPR-mediated deregulation of Bcl-2 family members.
|
29520102 |
2018 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
We previously developed cell-penetrating VDAC1-derived peptides that interact with hexokinase (HK), Bcl-2, and Bcl-xL to prevent the anti-apoptotic activities of these proteins and induce cancer cell death, with a focus on leukemia and glioblastoma.
|
29698587 |
2018 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Dual Inhibition of Bcl-2/Bcl-xL and XPO1 is synthetically lethal in glioblastoma model systems.
|
30337641 |
2018 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
On the other hand, the levels of miR-1271 were inversely related to the levels of Bcl-2, which have been significantly increased in GBM samples.
|
30248541 |
2018 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
MAO-B inhibitors selegiline and rasagiline protect neurons via increase expression of anti-apoptotic Bcl-2 and pro-survival neurotrophic factors in human neuroblastoma SH-SY5Y and glioblastoma U118MG cell lines.
|
29279995 |
2018 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The inhibition of both SH-SY5Y and U87MG cell proliferation was associated with an increase in the thiosulfate level, the number of cells with the inactive form of Bcl-2 protein, and with a decrease of mitochondrial membrane potential.
|
29508061 |
2018 |
|
Glioblastoma Multiforme
|
0.100 |
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
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, the expression levels of the Bcl-2 anti-apoptotic protein was significantly decreased while Bax and caspase-3 expression were both increased in glioblastoma cells (all, p<0.05).
|
29940755 |
2018 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
There were higher expressions of XIAP (p = 0.0032) and Bcl-2 (p = 0.0351) in the glioblastoma samples compared to the control samples of normal brain.
|
29236891 |
2017 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results revealed that the Au PENPs were capable of delivering Bcl-2 siRNA to glioblastoma cells with an excellent transfection efficiency, leading to specific gene silencing in the target cells (22% and 25.5% Bcl-2 protein expression in vitro and in vivo, respectively) thanks to the RGD peptide-mediated targeting pathway.
|
27921110 |
2017 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Type B and A monoamine oxidase and their inhibitors regulate the gene expression of Bcl-2 and neurotrophic factors in human glioblastoma U118MG cells: different signal pathways for neuroprotection by selegiline and rasagiline.
|
28577058 |
2017 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings uncover a novel mechanism through which mitochondrial PKM2 phosphorylates Bcl2 and inhibits apoptosis directly, highlight the essential role of PKM2 in ROS adaptation of cancer cells, and implicate HSP90-PKM2-Bcl2 axis as a potential target for therapeutic intervention in glioblastoma.
|
28035139 |
2017 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Hypoxic regions of GBM also highly express the pro-cell death Bcl-2 family member BNIP3, yet when BNIP3 is overexpressed in glioma cells, it induces cell death.
|
26467103 |
2016 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
MicroRNA-138 promotes acquired alkylator resistance in glioblastoma by targeting the Bcl-2-interacting mediator BIM.
|
26887050 |
2016 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
TP53 mutated glioblastoma stem-like cell cultures are sensitive to dual mTORC1/2 inhibition while resistance in TP53 wild type cultures can be overcome by combined inhibition of mTORC1/2 and Bcl-2.
|
27533080 |
2016 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Bcl-2 and the closely related Bcl-xL and Mcl-1 are often overexpressed in glioblastoma cells.
|
26775694 |
2016 |