Current gene co-expression databases and correlation networks do not support cell-specific analysis. Gene co-expression and expression correlation are subtly different phenomena, although both are likely to be functionally significant. Here, we report a new database, ImmuCo (http://immuco.bjmu.edu.cn), which is a cell-specific database that contains information about gene co-expression in immune cells, identifying co-expression and correlation between any two genes. The strength of co-expression of queried genes is indicated by signal values and detection calls, whereas expression correlation and strength are reflected by Pearson correlation coefficients. A scatter plot of the signal values is provided to directly illustrate the extent of co-expression and correlation. In addition, the database allows the analysis of cell-specific gene expression profile across multiple experimental conditions and can generate a list of genes that are highly correlated with the queried genes. Currently, the database covers 18 human cell groups and 10 mouse cell groups, including 20 283 human genes and 20 963 mouse genes. More than 8.6 × 108 and 7.4 × 108 probe set combinations are provided for querying each human and mouse cell group, respectively. Sample applications support the distinctive advantages of the database.
To detect the aberrantly expressed long non-coding RNAs in glioblastoma, two pairs of glioblastoma and adjacent normal tissues were firstly analyzed by RNA sequencing. Long intergenic non-coding RNA LINC00657 was considered to play a vital role in glioblastoma based on the results of RNA sequencing. Hence, we aimed to investigate the mechanisms by which LINC00657 regulated the tumorigenesis of glioblastoma. The level of LINC00657 in 40 glioblastoma samples and glioblastoma cell lines was detected by RT-qPCR. LINC00657 was significantly decreased in patients with glioblastoma compared with adjacent normal tissues. Overexpression of LINC00657 inhibited proliferation, colony formation, invasion and migration in glioma cells via inducing apoptosis. Dual luciferase report assay indicated LINC00657 was the target of miR-190a-3p. Overexpression of LINC00657 greatly inhibited the relative amount of miR-190a-3p. Besides, miR-190a-3p was found to be a negative regulator of PTEN. Additionally, active-caspase 3 was increased in cells transfected with pcDNA3.1-LINC00657. Finally, in vitro results were further confirmed by in vivo studies using nude mice bearing with glioblastoma tumors. In conclusion, LINC00657 was effective in inhibiting glioblastoma by acting as a molecular sponge of miR-190a-3p to regulate PTEN expression. Therefore, targeting LINC00657 may serve as a potential strategy for the treatment of patients with glioblastoma.
BackgroundWe conducted this meta-analysis based on eligible trials to investigate the relationship between phosphatase and tensin homolog (PTEN) genetic mutation and glioma patients’ survival.MethodsPubMed, Web of Science, and EMBASE were searched for eligible studies regarding the relationship between PTEN genetic mutation and glioma patients’ survival. The primary outcome was the overall survival of glioma patient with or without PTEN genetic mutation, and second outcome was prognostic factors for the survival of glioma patient. A fixed-effects or random-effects model was used to pool the estimates according to the heterogeneity among the included studies.ResultsNine cohort studies, involving 1,173 patients, were included in this meta-analysis. Pooled results suggested that glioma patients with PTEN genetic mutation had a significant shorter overall survival than those without PTEN genetic mutation (hazard ratio [HR] =2.23, 95% confidence interval [CI]: 1.35, 3.67; P=0.002). Furthermore, subgroup analysis indicated that this association was only observed in American patients (HR =2.19, 95% CI: 1.23, 3.89; P=0.008), but not in Chinese patients (HR =1.44, 95% CI: 0.29, 7.26; P=0.657). Histopathological grade (HR =1.42, 95% CI: 0.07, 28.41; P=0.818), age (HR =0.94, 95% CI: 0.43, 2.04; P=0.877), and sex (HR =1.28, 95% CI: 0.55, 2.98; P=0.564) were not significant prognostic factors for the survival of patients with glioma.ConclusionCurrent evidence indicates that PTEN genetic mutation is associated with poor prognosis in glioma patients. However, this finding is derived from data in observational studies, potentially subject to selection bias, and hence well conducted, high-quality randomized controlled trials are warranted.
Aloperine (ALO) exhibits neuroprotective effects against oxidative stress in vitro; however, its protective effect in early brain injury (EBI) following experimental subarachnoid hemorrhage (SAH) remains to be elucidated. The aim of the current study was to evaluate the antioxidant activity of ALO in EBI, and its association with nuclear factor erythroid-related factor 2 and the antioxidant responsive element (Nrf2-ARE) survival pathway. In the present study, an experimental SAH model was induced in rats following a prechiasmatic cistern injection. All rats were randomly divided into five groups: Sham, SAH, SAH+ vehicle, and an SAH+ ALO group (including low and high doses). ALO was administrated intraperitoneally at 2 and 24 h following induction of the SAH model. Brain samples were collected from each group at 48 h after SAH induction. Subsequently, western blotting, immunohistochemistry and cell apoptosis assays were performed, along with assessments for brain edema, neurological deficit, and the activity of oxidant/antioxidant factors. It was observed that the expression of Nrf2-ARE pathway-associated agents, including Nrf2, and heme oxygenase-1, were markedly increased in the high concentration ALO group compared with that of the SAH group. In addition, the level of oxidative damage was reduced. Furthermore, early brain damage, including brain edema, neurological deficit and cellular apoptosis were significantly ameliorated. In conclusion, the results of the present study indicate that ALO can ameliorate oxidative damage against EBI following SAH, most likely via the Nrf2-ARE survival pathway.
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