Harnessing oxidative stress for anti-glioma therapy

Ostrowski, Robert P.; Pucko, Emanuela

doi:10.1016/j.neuint.2022.105281

Cited by 15 publications

(16 citation statements)

References 199 publications

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“…In general, the increase in ROS levels is the cause of genetic and epigenetic mutations and proliferation signals [ 27 ]. The imbalance of ROS caused by antioxidants will cause cell death [ 15 , 16 ]. This study showed that PCBP2 reduced oxidative stress-induced apoptosis of glioma.…”

Section: Discussionmentioning

confidence: 99%

“…ROS is the normal product of an oxidation-reduction reaction in the body [ 14 ]. It is produced by normal metabolism or induced by exogenous factors such as smoking, radiation, and dust, causing lipid peroxidation, causing DNA strand breakage, oxidizing molecules in biofilm and tissue, and causing damage [ 15 ]. However, because the body can clear ROS to a certain extent, low-throughput ROS-mediated redox signals can regulate cell cycle and cell proliferation and play a central role.…”

Section: Introductionmentioning

confidence: 99%

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PCBP2 Reduced Oxidative Stress-Induced Apoptosis in Glioma through cGAS/STING Pathway by METTL3-Mediated m6A Modification

Chen

et al. 2022

Oxidative Medicine and Cellular Longevity

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Purpose. The most prevalent primary malignant tumor of CNS is glioma, which has a dismal prognosis. The theory of oxidative stress is one of the important theories in the study of its occurrence and development mechanism. In this study, the impacts of PCBP2 on glioma sufferers and the possible mechanisms were examined. Methods. Patients with glioma were obtained from May 2017 to July 2018. Quantitative PCR, microarray analysis, western blot analysis, and immunofluorescence were used in this experiment. Results. PCBP2 mRNA expression level and protein expression in patients with glioma were upregulated compared with paracancerous tissue. OS and DFS of PCBP2 low expression in patients with glioma were higher than those of PCBP2 high expression. PCBP2 promoted the progression and metastasis of glioma. PCBP2 reduced oxidative stress-induced apoptosis of glioma. PCBP2 suppressed the cGAS/STING pathway of glioma. PCBP2 protein interlinked with cGAS and cGAS was one target for PCBP2. METTL3-mediated m6A modification increases PCBP2 stability. Conclusion. Along the cGAS-STING signal pathway, PCBP2 decreased the apoptosis that oxidative stress-induced glioma caused, which might be a potential target to suppress oxidative stress-induced apoptosis of glioma.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

PCBP2 Reduced Oxidative Stress-Induced Apoptosis in Glioma through cGAS/STING Pathway by METTL3-Mediated m6A Modification

Chen

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…It has been found that peroxiredoxin 4 (PRDX4) is upregulated in glioma stem cells (GSC) in the central region of the tumor, resulting in low levels of ROS production in GSC even in a hypoxic environment 43 . Oxidative stress is also of considerable interest in the treatment of glioma 44 . Studies have shown that oxidative stress influences temozolomide resistance 43 and radiation therapy resistance 45 in glioma.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of oxidative stress-related lncRNA signatures in glioma reveals the discrepancy of prognostic and immune infiltration

Shi

Zhuo

et al. 2023

Sci Rep

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Oxidative stress refers to the process of reactive oxide species (ROS) increase in human body due to various factors, which leads to oxidative damage in human tissues. Current studies have confirmed that sustained oxidative stress is one of the distinctive features throughout the development of tumors. Numerous reports have shown that lncRNAs can regulate the process of oxidative stress through multiple pathways. However, the relationship between glioma-associated oxidative stress and lncRNAs is not clearly investigated. RNA sequencing data of GBM (glioblastoma) and LGG (low grade glioma) and corresponding clinical data were retrieved from the TCGA database. Oxidative stress related lncRNAs (ORLs) were identified by Pearson correlation analysis. Prognostic models for 6-ORLs were structured in the training cohort by univariate Cox regression analysis, multivariate Cox regression analysis and LASSO regression analysis. We constructed the nomogram and verified its predictive efficacy by Calibration curves and DCA decision curves. The biological functions and pathways of 6-ORLs-related mRNAs were inferred by Gene Set Enrichment Analysis. Immune cell abundance and immune function associated with risk score (RS) were estimated by ssGSEA, CIBERSORT and MCPcounter synthetically. External validation of the signature was completed using the CGGA-325 and CGGA-693 datasets. 6-ORLs signature—AC083864.2, AC107294.1, AL035446.1, CRNDE, LINC02600, and SNAI3-AS1—were identified through our analysis as being predictive of glioma prognosis. Kaplan–Meier and ROC curves indicated that the signature has a dependable predictive efficacy in the TCGA training cohort, validation cohort and CGGA-325/CGGA-693 test cohort. The 6-ORLs signature were verified to be independent prognostic predictors by multivariate cox regression and stratified survival analysis. Nomogram built with risk scores had strong predictive efficacy for patients' overall survival (OS). The outcomes of the functional enrichment analysis revealing potential molecular regulatory mechanisms for the 6-ORLs. Patients in the high-risk subgroup presented a significant immune microenvironment of macrophage M0 and cancer-associated fibroblast infiltration which was associated with a poorer prognosis. Finally, the expression levels of 6-ORLs in U87/U251/T98/U138 and HA1800 cell lines were verified by RT-qPCR. The nomogram in this study has been made available as a web version for clinicians. This 6-ORLs risk signature has the capabilities to predict the prognosis of glioma patients, assist in evaluating immune infiltration, and assess the efficacy of various anti-tumor systemic therapy regimens.

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“…Boric acid is an antioxidant substance due to its hydroxyl groups. The toxic effects of high doses of antioxidant substances on cells often prevent cell viability and result in apoptotic cell death 5 . In our design, we tried to examine the dose‐dependent effects of the function of boric acid as a chemotherapeutic agent on cell viability in C6 glioblastoma cells through ferroptosis and semaphorin signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

“…High doses of exogenous antioxidant compounds are hazardous to cancer cells whereas normal cells are unaffected. Side effects of chemotherapeutics can be reduced by inducing endogenous antioxidant capacity, and high‐dose therapeutic levels of ROS can inhibit the Warburg effect 5 . Therefore, new candidates for drugs targeting tumors, including gliomas, should regulate oxidative and inflammation signaling pathways, triggering apoptosis, which is known as a programmed cell death mechanism.…”

Section: Introductionmentioning

confidence: 99%

The dual role of boron in vitro neurotoxication of glioblastoma cells via SEMA3F/NRP2 and ferroptosis signaling pathways

Kar¹,

Hacıoğlu

Kaçar

2022

Environmental Toxicology

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Glioblastoma multiform (GBM) is a malignant tumor cancer that originates from the star‐shaped glial support tissues, namely astrocytes, and it is associated with a poor prognosis in the brain. The GBM has no cure, and chemotherapy, radiation therapy, and immunotherapy are all ineffective. A certain dose of Boric acid (BA) has many biochemical effects, conspicuously over antioxidant/oxidant rates. This article sought to investigate the modifies of various doses of BA on the glioblastoma concerning cytotoxicity, ferroptosis, apoptosis, and semaphorin–neuropilin signaling pathway. The Cytotoxic activity and cell viability of BA (0.39–25 mM) in C6 cells were tested at 24, 48, and 72 h using 3‐(4,5‐dimethylthiazol, 2‐yl)‐2,5‐diphenyl tetrazolium bromide (MTT). The IC50 concentration of BA at 1.56 mM was found and cell lysate used for biochemical analysis. Glutathione peroxidase 4 (GPx4) and ACLS4 levels of ferroptosis, levels of total antioxidant (TAS) and oxidant (TAS) parameters, malondialdehyde (MDA), apoptotic proteins as caspase 3 (CASP3) and caspase 7 (CASP7) were measured. The ferroptosis, semaphoring–neuropilin, apoptotic pathway markers and cell counts were analyzed with flow cytometry, Q‐PCR, Western and Elisa technique in the C6 cell lysate. BA triggered ferroptosis in the C6 cells dose‐dependently, affecting the semaphorin pathway, so reducing proliferation with apoptotic compared with untreated cell as control group (p < .05). This study revealed that BA, defined as trace element and natural compound, incubated ferroptosis, total oxidant molecules, and caspase protein in a dose‐dependently by disrupting SEMA3F in tumor cells.

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Harnessing oxidative stress for anti-glioma therapy

Cited by 15 publications

References 199 publications

PCBP2 Reduced Oxidative Stress-Induced Apoptosis in Glioma through cGAS/STING Pathway by METTL3-Mediated m6A Modification

PCBP2 Reduced Oxidative Stress-Induced Apoptosis in Glioma through cGAS/STING Pathway by METTL3-Mediated m6A Modification

Comprehensive analysis of oxidative stress-related lncRNA signatures in glioma reveals the discrepancy of prognostic and immune infiltration

The dual role of boron in vitro neurotoxication of glioblastoma cells via SEMA3F/NRP2 and ferroptosis signaling pathways

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