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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