IntroductionGliomas are the most frequent primary tumors in the human brain. Recent studies have identified a class of long noncoding RNAs, named lncRNAs, which were reported to participate in regulating the development of various diseases, including gliomas. In our previous studies, we found that lncRNA UBE2CP3-001 was overexpressed in gliomas but not in normal tissue. However, the molecular functions of UBE2CP3-001 in glioma are largely unknown.Material and methodsThe presence of UBE2CP3-001 in U87 cells, glioma tissues and normal brain tissues was detected by real-time RT-PCR. The ability of U87 cells to migrate was analyzed using a cellular wound healing assay after downregulation of UBE2CP3-001. The survival rate of U87 cells after UBE2CP3-001 knockdown was also analyzed using the CCK8 assay. In vivo tumor weights from xenograft tumors transfected with UBE2CP3-001 shRNA were further analyzed using in vivo animal experiments. The expression levels of MMP-9 and TRAF3IP2 were determined by Western blot.ResultsOur data showed that UBE2CP3-001 was overexpressed in most glioma tissues (p < 0.01). Downregulation of UBE2CP3-001 could inhibit cell migration (p < 0.01) and invasiveness (p < 0.01) of U87 cells. Downregulation of UBE2CP3-001 in U87 cells also suppressed the cell proliferation (p < 0.01) and promoted apoptosis (p < 0.01). Furthermore, in vivo studies confirmed that knockdown of UBE2CP3-001 could retard the growth of U87 xenograft tumors (p < 0.01). Western blot analysis showed that knockdown of UBE2CP3-001 could effectively inhibit the expression of MMP-9 (p < 0.01) and TRAF3IP2 (p < 0.01) in U87 glioma cells.ConclusionsThese data suggest an important role of UBE2CP3-001 in glioma and indicate its potential application in anti-glioma therapy.

Capsaicin is recognized as a natural tumor preventive compound and exhibits a remarkable anticancer action. Strong inhibitory role of capsaicin on gliomas has been well documented. However, the use of capsaicin is limited due to its hydrophobicity, low affinity, and short half-life. The present study aimed to explore the physiochemical characteristics of the capsaicin-loading nanoparticles prepared by methoxy polyethylene glycol-poly(caprolactone) (mPEG-PCL) amphiphilic block copolymer. It also aimed to evaluate the ability of the nanoparticles to cross the blood-brain barrier. Additionally, the uptake of nanoparticles in the glioma cells and its ability to inhibit cell proliferation were tested in human glioblastoma U251 cells. mPEG-PCL amphiphilic block copolymer was synthesized using the ring-opening polymerization method, and the capsaicin-loading nanoparticles were prepared with the solvent diffusion method. In vitro drug release assay revealed that the capsaicin-loading nanoparticles presented a slow-release characteristic. Coculture of the human glioblastoma U251 cells and the fluorescein-loading nanoparticles showed the uptake of nanoparticles in U251 cells by endocytosis. We found that the NIR-797 isothiocyanate-loading nanoparticles can cross the blood-brain barrier. In addition, the capsaicin-loading nanoparticle showed a remarkable inhibition on the growth of U251 cells. The efficacy of the capsaicin-loading nanoparticles against tumor cells was significantly superior to the capsaicin at low concentrations. It is concluded that the capsaicin-loading nanoparticles can provide an extremely promising approach for chemotherapy of gliomas.

Introduction: Aberrant expression of long non-coding RNAs (lncRNAs) has been implicated in various diseases, including cancer. However, little is known about lncRNAs in human brain gliomas. Material and methods: We examined lncRNA profiles from three glioma specimens using lncRNA expression profiling microarrays. Quantitative real-time RT-PCR was used to analyze the differential expression of raw intensities of lncRNA expression in glioma and peritumoral tissues. Results: We found 4858 lncRNAs to be differentially expressed between tumor tissue and peritumoral tissue. Of these, 2845 lncRNAs were up-regulated (fold change > 3.0) and 2013 were down-regulated (fold change < 1/3). A total of 4084 messenger RNAs were also differentially expressed, including 2280 up-regulated transcripts (fold change > 3.0) and 1804 that were down-regulated (fold change < 1/3). Consistent with the microarray data, qPCR confirmed differential expression of these 6 lncRNAs (ak125809, ak098473, uc002ehu.1, bc043564, NR_027322, and uc003qmb.2) between tumor and peritumoral tissue. We next established co-expression networks of differentially expressed lncRNAs and mRNAs. Many mRNAs, such as LOC729991, NUDCD1, SHC3, PDGFA, and MDM2, and lncRNAs, such as ENST00000425922, ENST00000455568, uc002ukz.1, ENST00000502715, and NR_027873, have been shown to play important roles in glioma development. Consistent with this, pathway analysis revealed that "GLIOMA" (KEGG Pathway ID: hsa05214) was significantly enriched in tumor tissue. Conclusions: Our data suggest that altered expression of lncRNAs may be a critical determinant of tumorigenesis in glioma patients.

Objective: Chronic subdural hematoma (CSDH) is a common form of intracranial hemorrhage with a substantial recurrence rate. Atorvastatin may reduce CSDH via its anti-inflammatory and pro-angiogenesis effects, but its effectiveness for preventing recurrent CSDH has never been explored. We hypothesized that atorvastatin is effective in reducing recurrence of CSDH after surgery and identified determining factors predictive of hematoma recurrence.Methods: A prospective study was conducted in 168 surgical cases of CSDH.All patients were randomly assigned to the group treated with atorvastatin or control group. Clinically relevant data were compared between two groups, and subsequently between the recurrence and non-recurrence patients. Multiple logistic regression analysis of the relationship between atorvastatin treatment and the recurrence using brain atrophy, septated and bilateral hematoma was performed.Results: Atorvastatin group conferred an advantage by significantly decreasing the recurrence rate (P = 0.023), and patients managed with atorvastatin also had a longer time-to-recurrence (P = 0.038). Admission brain atrophy and bilateral hematoma differed significantly between the recurrence and non-recurrence patients (P = 0.047 and P = 0.045). The results of logistic regression analysis showed that atorvastatin significantly reduced the probability of recurrence; severe brain atrophy and bilateral hematoma were independent risk factors for recurrent CSDH.Conclusions: Atorvastatin administration may decrease the risks of recurrence.Patients with severe brain atrophy and bilateral CSDH are prone to the recurrence.