[Retracted] Long non­coding RNA RNCR3 promotes glioma progression involving the Akt/GSK­3ß pathway.

[This retracts the article DOI: 10.3892/ol.2019.11002.].

Long non-coding RNA RNCR3 promotes glioma progression involving the Akt/GSK-3ß pathway.

Increasing evidence has confirmed that long non-coding RNAs (lncRNAs) serve critical roles in the development of a large number of human malignancies, including glioma. Several previously published studies have reported that the lncRNA retinal non-coding RNA3 (RNCR3; also termed LINC00599) exerts important roles in certain human malignancies; however, the precise biological role and underlying molecular mechanisms of RNCR3 in the development of glioma are yet to be fully elucidated. In the present study, it was revealed that the expression of RNCR3 was increased in glioma tissues compared with in corresponding adjacent normal tissues. Furthermore, increased levels of RNCR3 expression were associated with tumor progression and poor survival rates of patients with glioma. In addition, the U87 and U251 cell lines were selected to investigate the biological function and potential mechanisms of RNCR3 in glioma, and it was observed that RNCR3 knockdown led to an impairment of the proliferative and invasive abilities of cells; furthermore, G1 phase arrest was induced in glioma cells in vitro. Finally, the results of western blot analyses revealed that knockdown of RNCR3 led to a decrease in the expression levels of phosphorylated Akt and glycogen synthase kinase-3ß (GSK-3ß), without any clear effect on the expression levels of total Akt and GSK-3ß. Collectively, these results suggested that RNCR3 is able to regulate cell proliferation, the cell cycle and cell invasion in glioma, potentially via the Akt/GSK-3ß signaling pathway.

Interference with Protease-activated Receptor 1 Alleviates Neuronal Cell Death Induced by Lipopolysaccharide-Stimulated Microglial Cells through the PI3K/Akt Pathway.

Excessive microglial cells activation in response to inflammatory stimuli leads to synaptic loss, dysfunction, and neuronal cell death. Activated microglia are involved in the pathogenesis of neurological conditions and frequently contribute to several complications. Accumulating evidence suggests that signaling through PAR-1 is involved in inflammation, however, its function has yet to be fully elucidated. Here, we have demonstrated that the suppression of PAR-1 leads to down-regulation of inflammatory factors including IL-1ß, IL-6, TNF-α, NO, as well as the prevention of activation of NF-κB in BV2 cells. In addition, we found that a PAR-1 antagonist, SCH, prevented LPS-induced excessive microglial activation in a dose-dependent manner. As a result of SCH treatment, neuronal cell death via up-regulation of Akt-mediated pathways was reduced. Our results demonstrate that the beneficial effects of SCH are linked to its ability to block an inflammatory response. Further, we found that SCH inhibited the death of PC12 neurons from the cytotoxicity of activated BV2 cells via activation of the PI3K/Akt pathway. These neuro-protective effects appear to be related to inhibition of PAR-1, and represents a novel neuroprotective strategy that could has potential for use in therapeutic interventions of neuroinflammatory disease.

miR-193b promotes cell proliferation by targeting Smad3 in human glioma.

Studies have shown that several miRNAs play important roles in regulating a variety of cellular processes in gliomas. In these reports, upregulation of miR-193b has been found to be associated with a poor prognosis for glioma, but its functional mechanism in glioma remains unclear. This study investigates the roles of miR-193b in glioma tumor growth. We first showed that the expression of miR-193b was elevated in both glioma samples and glioma cells. Furthermore, downregulation of miR-193b by inhibitors was statistically correlated with a decrease in cell growth and a restored G1 accumulation. Luciferase assay and Western blot analysis revealed that Smad3 is a direct target of miR-193b. To prove that miR-193b regulated cell growth through the transforming growth factor-ß (TGF-ß) pathway in glioma cells by regulating Smad3, we tested endogenous targets of the TGF-ß pathway by measuring the accumulation of p21 mRNAs after downregulation of miR-193b. The results confirmed that induction of p21 was promoted by miR-193b inhibitors in glioma cells, although this induction disappeared when Smad3 was knocked down with siRNA. Moreover, downregulation of Smad3 mitigates the miR-193b suppression of glioma proliferation. In conclusion, these results suggest that miR-193b regulated cell growth in glioma through the TGF-ß pathway by regulating Smad3. Thus, our study indicates that miR-193b promotes cell proliferation by targeting Smad3 in human glioma, which may serve as a potentially useful target for development of miRNA-based therapies in the future.

Impaired white-matter integrity in photosensitive epilepsy: a DTI study using tract-based spatial statistics.

BACKGROUND AND PURPOSE: The present study was designed to map alterations in brain white-matter in photosensitive epilepsy (PSE) by applying tract-based spatial statistics (TBSS) analysis. METHODS: Diffusion tensor-imaging (DTI) data from MRI brain scans were collected from eight PSE patients and 16 gender- and age-matched non-epileptic controls using a SIEMENS Trio 3.0-Tesla scanner. For the white-matter analysis, DTI scans were processed using FSL software (http://www.fmrib.ox.ac.uk/fsl/index.html). Fractional anisotropy (FA) values in the PSE and control groups were compared using TBSS analysis corrected for multiple comparisons using threshold-free cluster enhancement. RESULTS: Compared with the control subjects, the corpus callosum of PSE patients had significantly lower FA values. CONCLUSION: Our DTI study indicates that white-matter in the corpus callosum was abnormal in PSE patients, and that DTI methods can serve as useful non-invasive tools to evaluate white-matter changes in PSE patients.

Total resection of a solitary fibrous tumor of the sellar diaphragm: A case report.

The present study reports the case of a patient with a vision impairment in the right eye. Head computed tomography revealed a round, hyperdense mass in the sellar and suprasellar regions. Pituitary gland magnetic resonance imaging (MRI) revealed isointensity on T1- and T2-weighted imaging. Tumor-enhanced scanning showed heterogeneous contrast enhancement. The initial diagnosis was that of meningioma or pituitary tumor. A total tumor resection was performed using a right pterional approach under general anesthesia. During surgery, the base of the tumor was located on the sellar diaphragm of the left anterior pituitary stalk. The pathological diagnosis was of a solitary fibrous tumor (SFT). The patient had no post-operative diabetes insipidus or idiopathic pituitary hypofunction. The clinical experience, imaging information and pathological features of SFT in this case report may provide a reference for correct diagnosis and total resection of SFTs in the sella turcica.

Biodegradable flow-diverting device for the treatment of intracranial aneurysm: short-term results of a rabbit experiment.

INTRODUCTION: One main complication of a flow-diverting device (FD) in treating intracranial aneurysm is stenosis of parent artery (PA) or occlusion of side branches. The use of a biodegradable device may satisfy the need for aneurysm occlusion and eliminate potential complications. METHODS: Twenty elastase-induced aneurysm rabbit models were divided into three groups: in group 1 (n = 7), polyglycolic acid FDs (PGA-FDs) were implanted across the necks of aneurysms and the abdominal aortas (AA), covering the ostium of a lumbar artery; in group 2 (n = 7), the PGA-FDs were replaced by metal FDs; and in group 3 (n = 6), the PGA-FDs were only implanted across the necks of aneurysms. Animals in group 3 underwent angiography at 6 weeks; those in groups 1 and 2 underwent angiography at 3 months. The status of aneurysm embolization and patency of side branches were assessed. RESULTS: Complete aneurysm occlusion rates in groups 1 and 3 were 83.3 and 66.7 %, respectively, compared with 0 % in group 2. No side branch occlusions were noted. PA neointimal hyperplasia was minimal, and there were no significant differences between groups 1 and 2 (P = 0.233). The neointimal coverage ratio of the branch ostium in AA in group 1 was not significantly different from that in group 2 (P = 0.605). The neointima comprised predominantly smooth muscle cells and collagen fibers. CONCLUSIONS: The PGA-FD was an effective device for the treatment of aneurysms and was safe for side branches at the 3-month follow-up.