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Dual inhibition of CPT1A and G6PD suppresses glioblastoma tumorspheres
ConclusionOur collective findings support the utility of dual suppression of CPT1A and G6PD with selective inhibitors, etomoxir and DHEA, as an efficacious therapeutic approach for GBM.
Source: Journal of Neuro-Oncology - November 17, 2022 Category: Cancer & Oncology Source Type: research

CBX3 promotes glioma U87 cell proliferation and predicts an unfavorable prognosis
ConclusionsIn conclusion, results of the current research suggest that a high CBX3 expression level predicts the poor prognosis for glioma patients. CBX3 can stimulate the growth of glioma U87 cells through targeting CDKN1A and CBX3 may become a novel target in the clinical treatment for glioma.
Source: Journal of Neuro-Oncology - September 8, 2019 Category: Cancer & Oncology Source Type: research

Activation of STAT1 by the FRK tyrosine kinase is associated with human glioma growth
ConclusionsOur findings highlighted a critical role of FRK in tumor suppression ability through promoting STAT1 activation, and provided a potential therapeutic target for glioma.
Source: Journal of Neuro-Oncology - April 15, 2019 Category: Cancer & Oncology Source Type: research

Functional relevance of genes predicted to be affected by epigenetic alterations in atypical teratoid/rhabdoid tumors
ConclusionsThese results suggest that a subset of genes affected by differential histone modification in ATRT is involved in the detrimental effects of SMARCB1-deficiency and also relevant in the biology of ATRT.
Source: Journal of Neuro-Oncology - November 16, 2018 Category: Cancer & Oncology Source Type: research

SALL4 suppresses PTEN expression to promote glioma cell proliferation via PI3K/AKT signaling pathway
AbstractSpalt-like transcription factor 4 (SALL4), a oncogene, is known to participate in multiple carcinomas, and is up-regulated in glioma. However, its actual role and underlying mechanisms in the development of glioma remain unclear. The present study explored the molecular functions of SALL4 in promoting cell proliferation in glioma. The expression level of SALL4 in 69  human glioma samples and six non-tumor brain tissues was determined using real-time polymerase chain reaction (PCR). Then, we transfected U87 and U251 cell lines with siRNA, and assessed cellular proliferation and cell cycle to understand the function...
Source: Journal of Neuro-Oncology - September 8, 2017 Category: Cancer & Oncology Source Type: research

Functional analysis of the DEPDC1 oncoantigen in malignant glioma and brain tumor initiating cells
AbstractDEP domain containing 1 (DEPDC1) is a novel oncoantigen expressed in cancer cells, which presents oncogenic activity and high immunogenicity. Although DEPDC1 has been predicted to be a useful antigen for the development of a cancer vaccine, its pathophysiological roles in glioma have not been investigated. Here, we analyzed the expression and function of DEPDC1 in malignant glioma. DEPDC1 expression in glioma cell lines, glioma tissues, and brain tumor initiating cells (BTICs) was assessed by western blot and quantitative polymerase chain reaction (PCR). The effect of DEPDC1 downregulation on cell growth and nuclea...
Source: Journal of Neuro-Oncology - May 29, 2017 Category: Cancer & Oncology Source Type: research

Protein kinase CK2 is important for the function of glioblastoma brain tumor initiating cells
In this study, the role of CK2 signaling in BTIC function was examined. We found that expression of CK2α was increased in CD133+ BTICs compared to CD133− cells within the same GBM xenolines. Treatment with CX-4945, an ATP-competitive inhibitor of CK2, led to reduced expression of Sox2 and Nestin, transcription factors important for the maintenance of stem cells. Similarly, inhibition of CK2 also reduced the frequency of CD133+ BTICs over the course of 7 days, indicating a role for CK2 in BTIC persistence and survival. Importantly, using an in vitro limiting dilution assay, we found that inhibition of CK2 kinase activity...
Source: Journal of Neuro-Oncology - February 7, 2017 Category: Cancer & Oncology Source Type: research

SMAD dependent signaling plays a detrimental role in a fly model of SMARCB1-deficiency and the biology of atypical teratoid/rhabdoid tumors
AbstractAtypical teratoid/rhabdoid tumors (ATRT) are highly malignant brain tumors arising in young children. The majority of ATRT is characterized by inactivation of the chromatin remodeling complex member SMARCB1 (INI1/hSNF5). Little is known, however, on downstream pathways involved in the detrimental effects of SMARCB1 deficiency which might also represent targets for treatment. UsingDrosophila melanogaster and the Gal4-UAS system, modifier screens were performed in order to identify the role of SMAD dependent signaling in the lethal phenotype associated with knockdown ofsnr1, the fly homolog ofSMARCB1. Expression and ...
Source: Journal of Neuro-Oncology - January 19, 2017 Category: Cancer & Oncology Source Type: research

Combined inhibition of vascular endothelial growth factor receptor signaling with temozolomide enhances cytotoxicity against human glioblastoma cells via downregulation of Neuropilin-1
Abstract Glioblastoma multiforme (GBM) is the most common and aggressive type of primary brain tumor with grave prognosis. Despite the growing understanding of the complex signaling networks responsible for the initiation and progression of GBM, many experimental therapies have fallen short of their treatment goals. In the present study, we investigated the novel molecular mechanisms responsible for synergistic action of temozolomide (TMZ) and anti-VEGF therapy in GBM cells. We tested the combined effects of TMZ and VEGF blockade in four human GBM cell lines: TMZ-sensitive U251-MG and U373-MG cells, and TMZ-resist...
Source: Journal of Neuro-Oncology - March 7, 2016 Category: Cancer & Oncology Source Type: research

Reactive oxygen species production has a critical role in hypoxia-induced Stat3 activation and angiogenesis in human glioblastoma
In this study, we explored the possible implication of reactive oxygen species (ROS) in hypoxia-driven Stat3 activation in human glioblastoma. We found that hypoxic stress increased ROS production as well as Stat3 activation and that ROS inhibitors (diphenyleneiodonium, rotenone and myxothiazol) and an antioxidant (N-acetyl-l-cysteine) blocked Stat3 activation under hypoxic conditions. To determine a major route of ROS production, we tested whether nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) is involved in hypoxia-induced ROS production. Nox4 expression was found to be increased at both mRNA and protein le...
Source: Journal of Neuro-Oncology - August 21, 2015 Category: Cancer & Oncology Source Type: research

Blocking the bFGF/STAT3 interaction through specific signaling pathways induces apoptosis in glioblastoma cells
In this study, we used inhibitors to block specific signaling pathways, including JAK, PI3K/Akt, and Src pathways, to explore how bFGF mediates crosstalk with STAT3 in two glioblastoma(GBM) cell lines: U251 (mutant p53) and U87 (wild-type p53). Furthermore, we explored how the bFGF/STAT3 pathway affects GBM cell apoptosis. Our results suggest that bFGF can induce the activation of STAT3 mainly through the JAK and PI3K/Akt pathways, and that siRNA-mediated knockdown of STAT3 markedly reduces the bFGF levels in U251 cells. Our results also suggest that STAT3 knockdown increases the expression of pro-apoptotic genes and decre...
Source: Journal of Neuro-Oncology - September 27, 2014 Category: Cancer & Oncology Source Type: research