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Numerous studies have reported that long noncoding RNA (lncRNA) dysregulation is involved in the progression of many malignant tumors, including glioma. The lncRNA ZNFX1 antisense RNA 1 (ZFAS1) plays an oncogenic role in various malignant tumors, such as gastric cancer and hepatocellular carcinoma. However, the underlying molecular mechanism of ZFAS1 in glioma has not been fully clarified. In this study, we found that the expression of ZFAS1 was upregulated in both glioma tissues and cell lines. Functional experiments revealed that ZFAS1 promoted glioma proliferation, migration and invasion, and increased resistance to temozolomide in vitro. By using online databases, RNA pull‐down assays and luciferase reporter assays, ZFAS1 was demonstrated to act as a sponge of miR‐150‐5p. Furthermore, proteolipid protein 2 (PLP2) was shown to be the functional target of miR‐150‐5p. Rescue experiments revealed that ZFAS1 regulated the expression of PLP2 by sponging miR‐150‐5p. Finally, a xenograft tumor assay demonstrated that ZFAS1 promoted glioma growth in vivo. Our results showed that ZFAS1 promoted glioma malignant progression by regulating the miR‐150‐5p/PLP2 axis, which may provide a potential therapeutic target for the treatment of glioma. [ABSTRACT FROM AUTHOR]

Vestibular schwannomas are rare intracranial tumors originating from Schwann cells of the vestibular nerve. Despite their benign nature, these tumors can exert significant mass effects and debilitating symptoms, including gradual hearing loss, vertigo, facial nerve dysfunction, and headaches. Current clinical management options encompass wait-and-scan, surgery, radiation therapy, and off-label medication. However, each approach exhibits its own challenges and harbors limitations that underscore the urgent need for therapeutic treatments. Over the past 2 decades, extensive elucidation of the molecular underpinnings of vestibular schwannomas has unraveled genetic anomalies, dysregulated signaling pathways, downstream of receptor tyrosine kinases, disrupted extracellular matrix, inflammatory tumor microenvironment, and altered cerebrospinal fluid composition as integral factors in driving the development and progression of the disease. Armed with this knowledge, novel therapeutic interventions tailored to the unique molecular characteristics of those conditions are actively being pursued. This review underscores the urgency of addressing the dearth of Food and Drug Administration-approved drugs for vestibular schwannoma, highlighting the key molecular discoveries and their potential translation into therapeutics. It provides an in-depth exploration of the evolving landscape of therapeutic development, which is currently advancing from bench to bedside. These ongoing efforts hold the promise of significantly transforming the lives of vestibular schwannoma patients in the future., Competing Interests: None declared., (© The Author(s) 2024. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.)

Long non-coding RNAs (lncRNAs) have great value in research on tumour targeted therapy, including for glioma. In the present study, we investigated the role of the lncRNA deleted in lymphocytic leukaemia 2 (lncRNA-DLEU2) in glioma. First, we found that lncRNA-DLEU2 is highly expressed in glioma tissues and cell lines. Next, experiments in cells showed that lncRNA-DLEU2 knockdown inhibited, whereas lncRNA-DLEU2 overexpression promoted, the clone formation, migration and invasion of glioma cells. A luciferase reporter assay and an RNA immunoprecipitation assay demonstrated that lncRNA-DLEU2 acts as a sponge for miR-186-5p in glioma cells. Further, studies suggested that miR-186-5p inhibits the expression of PDK3, which is an oncogene in glioma. Moreover, with rescue experiments, we demonstrated that lncRNA-DLEU2 regulates the expression of PDK3 and the progression of glioma in a miR-186-5p-dependent manner. Finally, we also showed that lncRNA-DLEU2 promotes glioma growth in a manner that is related to miR-186-5p and PDK3 in vivo . In conclusion, our study reported for the first time that lncRNA-DLEU2 promotes glioma progression by targeting the miR-186-5p/PDK3 axis. These findings provide novel strategies for the gene therapy treatment of glioma., Competing Interests: None.

Background: Gliomas are based on a genetic abnormality and present with a dismal prognosis. MicroRNAs (miRNAs) are considered to be important mediators of gene expression in glioma tissues., Methods: Real-time PCR was used to analyze the expression of microRNA-423-5p (miR-423-5p) in human glioma samples and normal brain tissue. Apoptosis, cell cycle, proliferation, immunostaining, transwell, in vitro 2D and 3D migration, and chemosensitivity assays were performed to assess the phenotypic changes in glioma cells overexpressing miRNA-423-5p. Western blotting was used to determine the expression of inhibitor of growth 4 (ING-4)in glioma tissues, and a luciferase reporter assay was conducted to confirm whether ING-4 is a direct target of miR-423-5p. Western blotting was used to identify the potential signaling pathways that are affected in glioma cell growth by miR-423-5p. Xenograft tumors were examined in vivo for the carcinogenic effects of miR-423-5p in glioma tissues., Results: We first reported that miR-423-5p expression was increased in gliomas and was a potential tumor promoter via targeting ING-4. The overexpression of miR-423-5p resulted in upregulation of important signaling molecules such as p-AKT and p-ERK1/2. In clinical samples, miR-423-5p was dysregulated, and a corresponding alteration in ING-4 expression was observed (P = .0207). Furthermore, the overexpression of miR-423-5p strengthened glioma cell proliferation, angiogenesis, and invasion. Finally, miR-423-5p overexpression also strengthened GBM neurosphere formation and rendered glioma cells resistant to temozolomide (TMZ)., Conclusion: This study establishes that miR-423-5p functions as an oncogene in glioma tissues by suppressing ING-4 and suggests that it has therapeutic potential for glioma., (© The Author(s) 2016. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)