Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In an attempt to understand the roles of several apoptosis-related genes in human glioma cells, the authors investigated the relationship of wild-type p53, interleukin-1beta-converting enzyme (ICE), caspase-3 (CPP32), bax, and bcl-2 to the apoptotic response of three glioma cell lines after treatment with etoposide.
|
10930016 |
2000 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Proteasome inhibitors were shown previously to induce mitochondria-independent and caspase-3-dependent apoptosis in human glioma cell lines by unknown mechanisms.
|
11522296 |
2001 |
Glioma
|
0.100 |
AlteredExpression
|
disease |
LHGDN |
The results were consistent with a block in the apoptotic signaling pathways of glioma cells between caspase-8 and caspase-3 activation, and that inducible Fadd could induce caspase-8 independent apoptosis in some cells.
|
15015772 |
2004 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The aim of the present study therefore was to deliver pro-apoptotic caspase-3 into malignant C6 glioma and immortalized rBCEC4 brain endothelial cells to induce cell death.
|
15690127 |
2005 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Using a caspase-3-activatable aminoluciferin, we were able to show the induction of apoptosis specifically in S-TRAIL vector-infected gliomas.
|
15922963 |
2005 |
Glioma
|
0.100 |
AlteredExpression
|
disease |
LHGDN |
In the present study, we retrospectively examined the immunohistochemical staining of cleaved caspase-3 (CC3), an activated form of caspase-3 that acts as a lethal protease at the most distal stage of the apoptosis pathway, in gliomas, and the correlation between the prognosis of patients and caspase-3 activation to find useful prognostic indicators.
|
17606719 |
2007 |
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Conversely, RNAi-mediated knockdown of alphaB-crystallin in Bcl2L12-expressing astrocytes and glioma cell lines with high endogenous alphaB-crystallin showed enhanced apoptosis, yet decreased necrotic cell death with associated increased caspase-3 but not caspase-7 activation.
|
18669646 |
2008 |
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Downregulation of XIAP resulted in activation of caspase-3 and caspase-9 to trigger apoptosis in glioma cells.
|
20676365 |
2010 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
While treatment with TRAIL alone caused partial processing of caspase-3 to its p20 intermediate in TRAIL-resistant glioma cell lines, co-treatment with TRAIL and subtoxic doses of paxilline caused complete processing of caspase-3 into its active subunits.
|
21150246 |
2011 |
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Overexpression of either of the four miRNAs in glioma cell lines reduced cell proliferation and/or increased caspase-3/7 activity.
|
26223576 |
2016 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here we could show that silencing of H1.5 triggered glioma cell apoptosis as evidenced by a marked increase in both the numbers of cleaved caspase-3(+) cells and in the amounts of cleaved PARP.
|
26559910 |
2015 |
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Interestingly, knockdown of PDAP-1 in combination with PDGF-B antibody inhibited glioma cell proliferation through activation of Caspase 3/7 and 9.
|
27448842 |
2016 |
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, we identified the activity of nitric oxide synthase 2 (NOS2, also known as iNOS) originating from the glioma cells as a driving stimulus in the control of microglial caspase-3 activity.
|
27618552 |
2016 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In general, such ranking corresponded to a scale of pro-apoptotic impairments in the morphology of glioma U251 cells and the results of Western-blot analysis of cleaved Caspase 3.
|
28409498 |
2017 |
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In vitro results showed that UA decreased glioma cell numbers, increased the sub-G1 fraction and induced apoptotic death, accompanied by increased active caspase-3 protein levels.
|
28663034 |
2017 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data indicated that linarin suppressed glioma cell proliferation and migration by inducing apoptosis, which was through reducing cell cycle-related signals, including Survivin, p-Rb, and Cyclin D1, while promoting p21, Bax, Caspase-3 and poly (ADP-ribose) polymerase (PARP) activation.
|
28858735 |
2017 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Synergistic and targeted therapy with a procaspase-3 activator and temozolomide extends survival in glioma rodent models and is feasible for the treatment of canine malignant glioma patients.
|
29113289 |
2017 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The study shows NC employing pDok2, caspase 3 dependent cell death in C6 rat glioma and U87 human malignant glioblastoma cells.
|
29329030 |
2018 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Both compounds exhibited selective cytotoxicity against human glioma stem cells (GSCs) and induced caspase-3 dependent extrinsic apoptosis by increasing the expression of interleukin 1 (IL-1), tumor necrosis factor (TNF-α), and the cleaved caspase-3, while damaged the unlimited proliferation and self-renewal capacity of GSCs.
|
29486949 |
2018 |
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The possible underlying mechanisms could be related to inhibiting telomerase activity, downregulating expression of Bcl-2 and hTERT, and upregulating expression of caspase-3 of human glioma U251 cells.
|
30260020 |
2019 |
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, FABP7 overexpression in U87 human glioma cell line revealed higher LD accumulation and higher antioxidant defence enzyme (TRX, TRX reductase 1 [TRXRD1]) expression than mock transfection and protected against apoptosis signalling (p38 MAPK, SAPK/JNK and cleaved caspase 3) activation.
|
30680690 |
2019 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
FINDINGS: The potential tumor suppressor role of SLC2A4RG was further validated by in vitro and in vivo experiments that SLC2A4RG could attenuate cell proliferation via G2/M phase arrest and induce glioma cell apoptosis by direct transactivation of caspase-3 and caspase-6.
|
30686753 |
2019 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Additionally, procaspase-3 expressing glioma and meningioma cell lines were sensitive to the apoptotic effects of PAC-1 at biologically relevant exposures achievable in cancer patients.
|
30859090 |
2019 |
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Then, we performed real-time PCR, CCK-8, colony formation assay, flow cytometry, caspase-3/7 assay and animal experiment to detect the function of ENST00000413528 in glioma after ENST00000413528 knockdown.
|
30924320 |
2019 |
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The molecule mechanism experiments revealed that SNHG16 could not only inhibit the expression of p21 but also suppressed the level of caspase 3 and 9, while promoted cyclinD1 and cyclinB1 expression. lncRNA SNHG16 could promote the cell proliferation and inhibit the apoptosis of glioma through suppressing p21, indicating that lncRNA SNHG16 might be quite vital for the diagnosis and progression of glioma and could even be a novel therapeutic target for glioma.
|
30972632 |
2019 |