ArticleOxidative medicine and cellular longevity2022
PCBP2 Reduced Oxidative Stress-Induced Apoptosis in Glioma through cGAS/STING Pathway by METTL3-Mediated m6A Modification.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- The STING Signaling: A Novel Target for Central Nervous System Diseases.Cellular and molecular neurobiology · 2025Review
- Role of M6a Methylation in Myocardial Ischemia-Reperfusion Injury and Doxorubicin-Induced Cardiotoxicity.Cardiovascular toxicology · 2024Review
- Progression of mCell death discovery · 2024Review
- Unraveling the independent role of METTL3 in m6A modification and tumor progression in esophageal squamous cell carcinoma.Scientific reports · 2024Article
- Harnessing innate immune pathways for therapeutic advancement in cancer.Signal transduction and targeted therapy · 2024Review
- Corosolic acid enhances oxidative stress-induced apoptosis and senescence in pancreatic cancer cells by inhibiting the JAK2/STAT3 pathway.Molecular biology reports · 2024Article
- MrGPS: an m6A-related gene pair signature to predict the prognosis and immunological impact of glioma patients.Briefings in bioinformatics · 2023Article
- Retracted: PCBP2 Reduced Oxidative Stress-Induced Apoptosis in Glioma through cGAS/STING Pathway by METTL3-Mediated m6A Modification.Oxidative medicine and cellular longevity · 2023Article
Corrections and comments
- Retraction · 2023-09-27Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Concerns/Issues about Referencing/Attributions · Concerns/Issues about Peer Review · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Computer-Aided Content or Computer-Generated Content · Unreliable Results and/or Conclusions · · See also: https://pubpeer.com/publications/0BDDEBFEC398B6576864945F3B5096
- Retracted
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
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