|
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 |
Biomarker
|
disease |
BEFREE |
In conclusion, this study suggested that miR-206 could act as a tumor suppressor gene through inhibiting BCL-2 in the development of glioblastoma.
|
27558109 |
2016 |
|
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 |
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
|
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 |
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
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Mcl-1, an antiapoptotic member of the Bcl-2 family, is overexpressed in human glioblastoma, conferring a survival advantage to tumor cells.
|
23551751 |
2013 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
MicroRNA-138 promotes acquired alkylator resistance in glioblastoma by targeting the Bcl-2-interacting mediator BIM.
|
26887050 |
2016 |
|
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 |
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 |
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
|
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
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data suggest that Bcl-2 confers resistance to mTORC1/2 inhibitors in TP53 wild type GSCs and that combined inhibition of both mTORC1/2 and Bcl-2 is worthwhile to explore further in TP53 wild type glioblastomas, whereas in TP53 mutated glioblastomas dual mTORC1/2 inhibitors should be explored.
|
27533080 |
2016 |
|
Glioblastoma
|
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
|
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
|
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 |
LHGDN |
p53, mdm2, EGFR, and msh2 expression in paired initial and recurrent glioblastoma multiforme.
|
12754350 |
2003 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
PI3K and Bcl-2 inhibition primes glioblastoma cells to apoptosis through downregulation of Mcl-1 and Phospho-BAD.
|
24757258 |
2014 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Previously, we established that microRNA-153 (miR-153) induces apoptosis by downregulating B-cell lymphoma 2 (Bcl-2) and myeloid cell leukemia sequence 1 (Mcl-1) protein expression levels in glioblastoma cell line DBTRG-05MG.
|
21213215 |
2011 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Prognostic impact of the expression/phosphorylation of the BH3-only proteins of the BCL-2 family in glioblastoma multiforme.
|
23152057 |
2012 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Recent data suggest that glioblastomas (GBM) activate the c-MET signaling pathway and display increased levels in anti-apoptotic Bcl-2 family members.
|
29743557 |
2018 |
|
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 |
|
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 |
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 |
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 |