Increasing evidence has indicated that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes, including glioma. However, the underlying mechanism of lncRNAs in gliomagenesis is still ambiguous. In this study, we aim to investigate the role of long intergenic noncoding RNA 00958 (LINC00958) in the tumorigenesis of glioma. Results revealed that LINC00958 was significantly upregulated in glioma tissues and cell lines compared with that of adjacent normal brain tissues and normal human astrocytes. Moreover, the ectopic overexpression of LINC00958 was correlated with poor prognosis of glioma patients. Loss-of-function experiments indicated that LINC00958 knockdown suppressed glioma cell proliferation, invasion, and induced cycle arrest at G0/G1 phase in vitro, and inhibited tumor growth in vivo. Bioinformatics programs and luciferase reporter assay revealed that miR-203 shared complementary binding sites with both 3'-untranslated region of LINC00958 and CDK2. In summary, our study concludes that LINC00958 acts as an oncogenic gene in the gliomagenesis through miR-203-CDK2 regulation, providing a novel insight into glioma tumorigenesis.

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Signal peptide CUB EGF-like domain-containing protein 2 (SCUBE2), a member of the SCUBE family of proteins, was recently found to play an important role in cancer development. However, little is known regarding its biological function in glioma. In the present study, we investigated the effect of SCUBE2 on glioma and explored its relevant mechanisms. The study showed that SCUBE2 had a low expression in glioma tissue and cell lines. SCUBE2 overexpression inhibited glioma cell proliferation in vitro and in vivo as well as suppressed glioma cell migration and invasion in vitro. Furthermore, we found that the Sonic hedgehog (Shh) signaling pathway was involved in the inhibitory effect of SCUBE2 overexpression on glioma cells. In light of the results obtained from our study, SCUBE2 may be regarded as a potential therapeutic target for glioma.

Background Intracerebral hemorrhage (ICH) causes neurotransmitter release, oligemia, membrane depolarization, mitochondrial dysfunction, and results in the high rate of mortality and functional disability. Here, we focus on PTEN‐induced kinase 1 (PINK1), a mitochondrial‐targeted protein kinase, and explore its role in ICH progression. Methods The qPCR and Western blot were performed to examine the expression of PINK1 in ICH patients and mouse model. PINK1 gain‐ and loss‐of‐function mice were used to evaluate their protective role on brain injury and behavioral disorders. Flow cytometry was carried out, mitochondrial membrane potential and reactive oxygen species production were detected to explore the distribution and neuroprotective function of PINK1. Results PINK1 mRNA was upregulated, however, its protein was downregulated in ICH patients. The reduction of PINK1 was mainly happened in microglial cells in ICH model. Overexpression of PINK1 is able to rescue ICH‐induced behavioral disorders. PINK1 protects ICH‐induced brain injury by promoting mitochondrial autophagy in microglia. Conclusion PINK1 possesses a neuroprotective role and antagonizes ICH by promoting mitochondrial autophagy, which may be of value as a therapeutic target for ICH treatment.

Cytoplasmic polyadenylation element-binding protein 4 (CPEB4) is a highly conserved, sequence-specific RNA-binding protein that recruits translational repression or cytoplasmic polyadenylation machinery to target mRNAs. Recent studies have shown that CPEBs are expressed in somatic tissues and have essential functions supporting tumor growth, vascularization, and invasion. Overexpression of CPEB4 has been reported in pancreatic ductal adenocarcinoma and is associated with poor prognoses. However, whether CPEB4 plays a role in the tumorigenesis of gliomas is unknown. Here, we analyzed the expression of CPEB4 in gliomas. The expression profiles of CPEB4 mRNA and protein in nine normal brain tissues and 63 gliomas were detected using immunohistochemistry, real-time PCR, and western blotting. CPEB4-positive expression was significantly correlated with the pathological grade of glioma; abundant expression was observed in high-grade gliomas, whereas little or no expression was observed in normal astrocytes. Immunohistochemistry staining indicated that CPEB4 was mainly localized in the cytoplasm. In addition, CPEB4 was more highly expressed in U87 glioma cells than in U251 cells. CPEB4 expression significantly correlated with the grade in clinical gliomas. This study suggested that CPEB4 might play a role in the pathogenesis of glioma.