MicroRNAs (miRNAs/miRs) have been revealed to influence the development and progression of glioblastoma. Although a number of miRNAs are abnormally expressed in glioblastoma it is not clear whether they are a factor associated with glioblastoma pathogenesis. In the present study, miR-7-5p was identified as being aberrantly downregulated in glioblastoma tissues and cell lines. miR-7-5p overexpression significantly decreased the migratory and invasive capacity of the cells, while miR-7-5p silencing had the opposite effect. In addition, a luciferase assay confirmed that special AT rich sequence binding protein 1 (SATB1) was a direct target gene of miR-7-5p in glioblastoma. The overexpression of SATB1 in glioblastoma was revealed to promote cell migration and invasion. In addition, SATB1 overexpression may weaken the inhibitory effect of miR-7-5p on cell migration and invasion. miR-7-5p overexpression reversed the effects of SATB1 on cell migration and invasion in glioblastoma cells. In conclusion, miR-7-5p may be a useful therapeutic target for the diagnosis and treatment of patients with glioblastoma.

Objective: This study aimed to investigate the neuroprotective effect of heme oxygenase-1 (HO-1) on the PI3K/AKT signaling pathway in rats with cerebral hemorrhage. Materials and methods: Adult male Sprague-Dawley rats were randomly divided into: a sham group, a model group and an HO-1 inhibitor group (ZnPP group). Functional defects after surgery were scored according to the Longa5 standard. Hemotoxylin and eosin staining was used to detect whether the model was constructed successfully. Superoxide dismutase (SOD) vitality and malondialdehyde (MDA) content were calculated by the xanthine oxidase method and thiobarbituric acid method, respectively. Blood-brain barrier permeability was measured by Evans Blue. Apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. The expression of Bcl-2 and BAX was evaluated by immunohistochemistry and the expression of PI3K, p-PI3K, AKT and p-AKT was tested by Western blotting. Results: The rat intracerebral hemorrhage model was successfully constructed. Compared with the model group, the bleeding in the ZnPP group was more serious, the cell edema and deformation were aggravated, and the neurological deficit score in the rat was significantly increased. In addition, the content of Evans blue, MDA, the number of apoptotic cells, the water content of brain tissue and the expression of BAX were significantly increased, while the SOD activity and the expressions of Bcl-2, p-PI3K and p-AKT protein were decreased. Conclusion: HO-1 could protect the nerves of rats with cerebral hemorrhage by regulating the PI3K/AKT signaling pathway.

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Glioma is the most common and rapidly progressive type of malignant primary brain tumor in adults. miR-153 plays a major role in many malignancies; nevertheless, few studies have been conducted on glioma. The aim of the present study was to explore the role of miR-153 and SNAI1 on invasion in glioma. Reverse transcription-quantitative PCR was employed to measure the expression levels of miR-153 and SNAI1 mRNA. Transwell assay was utilized to calculate the capacity of invasion. Luciferase report assay was applied to detect whether SNAI1 was a target of miR-153. miR-153 was downregulated in glioma tissues and cells versus paracancerous tissues and normal immortalized gliocyte HEB cells. Transwell assay was used to measure whether a low expression of miR-153 in glioma indicated inhibition of cell invasion. We verified that SNAI1 was a target of miR-153 and had a negative association with miR-153 detected by luciferase reporter assay. Additionally, miR-153 suppressed cell invasive ability by regulating SNAI1 expression, whose partial function was reversed by SNAI1. miR-153 suppressed cell invasion of glioma by directly targeting SNAI1. Thus, miR-153/SNAI1 axis may be a novel target for cervical cancer treatment.