|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
With regard to tumors of central nervous system origin, bcl2 expression was absent from most medulloblastomas but was detected at moderate to low levels in a retinoblastoma and some glioblastoma multiforme cell lines.
|
1742726 |
1991 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, these results indicate a role for Bag-1/Bcl-2 interactions in providing a survival advantage to cancer cells in a deprived microenvironment that may be characteristic of ischemic/hypoxic tumors such as human glioblastoma multiforme, and suggest that Bcl-2/Bag-1 interactions also modulate cell proliferation.
|
10764042 |
2000 |
|
Glioblastoma
|
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
|
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
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this study, we identified Mcl-1, an anti-apoptotic Bcl-2 family member, as a critical player involved in determining the sensitivity of GBM to TRAIL-induced apoptosis.
|
24213561 |
2014 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Bcl-2 and the closely related Bcl-xL and Mcl-1 are often overexpressed in glioblastoma cells.
|
26775694 |
2016 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, these results suggested that GMFβ-dependent inactivation of the ERK1/2-Bcl-2/survivin pathway mediated the antiproliferative effect of β-elemene on glioblastoma.
|
24866280 |
2014 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In the present study, we have analyzed tumors of two age-matched, equally treated groups of GBM patients with different postoperative time to tumor progression (TTP), defined as 'short-term' for TTP of less than 6 months (n = 54), and 'long-term' for TTP of more than 12 months (n = 39) for alterations in apoptosis regulatory pathways: Mutations of the TP53 tumor suppressor gene and/or nuclear accumulation of its gene product p53, expression of Waf/p21, CD95 (Apo1/Fas), and Bcl-2.
|
11519857 |
2001 |
|
Glioblastoma
|
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
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Here, we identify Bcl2-like 13 (Bcl2L13), an atypical member of the Bcl-2 family, as a therapy susceptibility gene with elevated expression in solid and blood cancers, including glioblastoma (GBM).
|
24706805 |
2014 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The cell death stimulus increased anti-apoptotic Bcl-2 and decreased pro-apoptotic Bcl-2 members (Bak and Bax) and Fas in glioblastoma cells deficient in DNA-PK.
|
15493013 |
2005 |
|
Glioblastoma
|
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
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Significant de-phosphorylation of Akt, increased Bax expression, decreased Bcl-2 expression and cleavage of caspase-3 were also observed in resveratrol-induced apoptosis in glioblastoma cells.
|
21743969 |
2011 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
High steady-state levels of Bcl-2 were identified as potentially accounting for the resistance of a proportion of glioblastoma lines to factors secreted by activated CTLs.
|
20483178 |
2010 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
LHGDN |
Our current study demonstrated that Bcl-2 siRNA significantly augmented taxol mediated apoptosis in different human glioblastoma cells through induction of calpain and caspase proteolytic activities.
|
18357521 |
2009 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Overexpression of FHL2 increased the tumorigenicity of glioblastoma cells in nude mice and decreased the mRNA levels of p53 and its downstream proapoptotic genes, including p21, Bcl2-associated protein X (Bax), and p53-upregulated modulator of apoptosis.
|
18615633 |
2008 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
BCL-2 family protein expression in initial and recurrent glioblastomas: modulation by radiochemotherapy.
|
10567494 |
1999 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Immunolabelling with the bcl-2 antibody was found in 44% of fibrillary astrocytomas, 42% of anaplastic astrocytomas, and 28% of glioblastomas.
|
7494604 |
1995 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our current study demonstrated that Bcl-2 siRNA significantly augmented taxol mediated apoptosis in different human glioblastoma cells through induction of calpain and caspase proteolytic activities.
|
18357521 |
2009 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Bcl-2 and Bax genes are probably involved in the reduction of malignancy of glioblastoma cell caused by the introduction of EGFR-antisense into these tumor cells.
|
10628370 |
2000 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Gemistocytes showed a significantly higher bcl-2 expression than all tumor cells, with a mean bcl-2 1 of 15.6% versus 2.7% in low-grade astrocytomas (p = 0.0004), 20.9% versus 3.0% in anaplastic astrocytoma (p = 0.002), and 30.2% versus 5.2% in glioblastomas (p = 0.0002).
|
9042164 |
1997 |
|
Glioblastoma
|
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
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Treatment of glioblastoma cells with Ro 31-8220 lead to a rapid decline in the level of the anti-apoptosis protein bcl-2.
|
9858877 |
1998 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Downregulation of bcl-2 and bcl-xl expression in glioblastoma cells can induce apoptosis.
|
19267218 |
2010 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Resistance to chemotherapy in glioblastoma has been linked to the expression of antiapoptotic Bcl-2 family members including Bcl-xL.
|
12218266 |
2002 |