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Resection of high-grade glioma with sodium fluorescein can improve the resection rate of the glioma and improve survival. However, it is unclear whether the yellow fluorescence boundary of the high-grade glioma is consistent with the actual boundary of the tumor. This study explores the yellow fluorescence boundary and the actual tumor boundary in high-grade glioma surgery. This is a retrospective analysis of 10 patients with high-grade gliomas who underwent tumor visualization with sodium fluorescein. After staining of the tumor, random selections of both developed and non-developed yellow fluorescent border tissue at the fluorescence chromogenic boundary were made, followed by pathological examination. Claudin-5, an important component of the tight connections between vascular endothelial cells, was assessed by immunohistochemistry and qRT-PCR in the tumor and surrounding tissues in order to determine the tumor cell content of the tissue, blood-brain barrier damage, and vascular proliferation. The yellow fluorescence boundary was compared with the actual tumor boundary and the results analyzed. Tumor cells were still detected outside the yellow fluorescence boundary during high-grade glioma surgery (P < 0.05). Claudin-5 expression was higher in high-grade gliomas than in adjacent normal tissues (P < 0.05), while disconnected Claudin-5 expression was associated with intraoperative yellow fluorescence imaging (r = 0.67). There is a difference between the yellow fluorescence boundary and the actual boundary of the tumor in high-grade glioma, and there are glioma cell infiltrations in the brain tissue of the undeveloped yellow fluorescent border. To ensure patient recovery and function, it is recommended that tumor resection be expanded based on yellow fluorescence visualization. Claudin-5 is overall up-regulated in high-grade gliomas, but some Claudin-5 expression is disconnected. This Claudin-5 expression pattern may be related to the development of yellow fluorescence. [ABSTRACT FROM AUTHOR]

• GAS5 and PTEN was downregulated in glioma and miR-106b was opposite. • GAS5 regulated the EMT process of glioma cells. • GAS5 directly targeted miR-106b in glioma. • PTEN was a target of miR-106b for regulating EMT process of glioma cells. LncRNA growth arrest special 5 (GAS5) and microRNA-106b (miR-106b) have been reported to be involved in the regulation of gliomas. However, their precise mechanisms in regulating the progression and development of gliomas remain unclear. We aimed to investigate the interaction between GAS5 and miR-106b, and their influence on the proliferation, migration, and invasion of gliomas cells. Western blotting and qRT-PCR were applied for measuring expression of protein and mRNA, respectively. The proliferation, migration, and invasion of cells were measured by MTT, wound healing, and transwell assays, respectively. Dual luciferase reporter assay was applied for confirming the binding site between miR-106b and GAS5, miR-106b and PTEN. Significant higher expression of miR-106b, and lower expression of GAS5 and PTEN in the glioma tissues were observed. The binding sites between GAS5 and miR-106b, miR-106b and PTEN were identified. GAS5 could regulate the expression of PTEN through targeting miR-106b, and further influence EMT process, and the proliferation, migration, and invasion of gliomas cells. Meanwhile, PTEN could remarkably inhibited the proliferation, migration and invasion of glioma cells. The influence of PTEN on glioma cells and EMT was similar to GAS5. GAS5 could regulate the EMT process, and the migration of gliomas cells through miR-106b targeting PTEN. Therefore, our findings may provide a new thought for the study of pathogenesis and treatment of glioma. [ABSTRACT FROM AUTHOR]