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Glioblastoma is a malignant brain tumor originating in the central nervous system. Successfully therapy of this disease required the efficient delivery of therapeutic agents to the tumor cells and tissues. Delivery of anticancer drugs using novel nanocarriers is promising in glioma treatment.Polymeric nanoparticles (PNPs), solid lipid nanoparticles (SLNs), and nanostructured lipid carriers (NLCs) were constructed for the delivery of temozolomide (TMZ). The anti-tumor effects of the three kinds of nanocarriers were compared to provide the optimum choice for gliomatosis cerebri treatment.TMZ-loaded PNPs (T-PNPs), SLNs (T-SLNs), and NLCs (T-NLCs) were formulated. Their particle size, zeta potential, drug encapsulation efficiency (EE), and drug loading (DL) capacity were evaluated. Anti-tumor efficacies of the three kinds of nanocarriers were evaluated on U87 malignant glioma cells (U87 MG cells) and mice-bearing malignant glioma model.T-NLCs displayed the best anti-tumor activity than other formulations in vivo and in vitro. The most significantly glioma inhibition was observed on NLCs formulations than PNPs and SLNs.This work demonstrates that NLCs can deliver TMZ into U87MG cells more efficiently, with higher inhibition efficacy than PNPs and SLNs. T-NLCs could be an excellent drug delivery system for glioblastoma chemotherapy.

MicroRNAs (miRNAs) are able to function as either oncogenes or tumor suppressor genes in tumorigenesis, and have been proposed as novel targets for anticancer treatment. It has previously been suggested that miRNAs have important roles in the initiation and progression of glioblastoma; however, the effects of miR‑566 in glioblastoma are currently unclear. The present study aimed to demonstrate that miR-566 can modulate vascular endothelial growth factor (VEGF) by targeting Von Hippel‑Lindau (VHL) in glioblastoma in vitro and in vivo by inhibiting the expression of miR-566. Glioblastoma is a highly vascularized tumor, which exhibits increased expression of angiogenic factors, including VEGF, which are crucial in the process of glioblastoma angiogenesis. Existing research has demonstrated that VHL is a tumor suppressor gene that is associated with various tumors. In addition, VHL is able to regulate the expression of VEGF by promoting the degradation of hypoxia‑inducible factor‑1α via ubiquitination. It has been predicted, using bioinformatics, that the VHL gene is regulated by miR‑566. Therefore, the present study hypothesized that miR‑566 may regulate VEGF expression by targeting VHL during the angiogenic process of glioblastoma multiforme. The results of the present study demonstrated that inhibition of miR‑566 expression increases the expression levels of VHL, decreases the expression levels of VEGF, and inhibits the invasive and migratory abilities of glioblastoma. In addition, VHL was identified as a functional target of miR‑566.

BACKGROUND Glutathione peroxidase 1 (GPX1) is an essential component of the intracellular antioxidant enzyme system, but little is known about the role of GPX1 in the progression of malignancy in gliomas. Using public datasets, this study investigated the prognostic role of GPX1 and immune infiltrates in glioma. MATERIAL AND METHODS We investigated GPX1 expression levels in different cancers using the ONCOMINE and Tumor Immune Estimation Resource (TIMER) datasets. We also explored the prognostic landscape of GPX1 in gliomas based on The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) datasets. Some significant pathways were identified by function enrichment analysis. We then explored the association between GPX1 expression and levels of tumor-infiltrating immune cells based on TIMER and Gene Expression Profiling Interactive Analysis (GEPIA) datasets. RESULTS Expression of GPX1 in brain and central nervous system cancers is at a much high level than in normal tissues, and it is higher in glioblastoma (GBM) than in lower-grade glioma (LGG). We found GPX1 expression to be positively correlated with the malignant clinicopathologic characteristics of gliomas. Univariate analysis and multivariate analysis revealed that overexpression of GPX1 was correlated with a worse prognosis in patients, and a nomogram indicated that GPX1 expression can predict clinical prognosis of glioma. Function enrichment analysis showed that some important pathways are related to glioma malignancy. Expression of GPX1 was positively associated with infiltrating levels of 6 types of immune cells and most of their gene markers in GBM and LGG. CONCLUSIONS These results indicate that GPX1 is an independent prognostic factor and a novel biomarker for predicting the progression of malignancy in gliomas, which is associated with immune infiltration.

The authors of the above article drew to our attention that they had identified three instances of data overlapping between data panels, suggesting that data purportedly showing results obtained under different experimental conditions had been derived from the same original source. Comparing between the two figures, two pairs of panels in Fig. 4B (the Mimics control and blank experiments for the U87 and U251 cell lines) were shown to be overlapping, and a further pair of panels showed overlapping data in Fig. 6B (the data panels for the miR‑375 mi + .pCDNA/RWDD3 and miR‑375 mi + .pCDNA experiments for the U87 cell line). The authors were able to re‑examine the original data files and retrieve the correct data panels. The errors in these figures arose through inadvertently assembling Figs. 4 and 6 incorrectly. The revised versions of Figs. 4 and 6, featuring the corrected data panels for the Mimics control and blank experiments for the U87 and U251 cell lines in Fig. 4B, and the correct data for the U87 cell line in Fig. 6B, are shown opposite and on the next page, respectively. Note that the corrections to the data shown in these Figures do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Oncology Reports 39: 1825-1834, 2018; DOI: 10.3892/or.2018.6261].

This study aimed to investigate the effect of interfering thyroid hormone receptor interacting protein 13 (TRIP13) expression on the proliferation, apoptosis and metastasis of thyroid cancer (TC) cells and the involved mechanisms. RT-PCR, immunohistochemical analysis and western blot found that compared with normal tissues, the expressions of TRIP13 and N-cadherin in TC tissues were significantly increased, while the expressions of tetratricopeptide repeat protein 5 (TTC5), p-p53 and E-cadherin were significantly decreased (P

The most common and aggressive type of brain cancer in adults is glioblastoma multiforme (GBM), and hypoxia is a common feature of glioblastoma. As the histological features of glioma include capillary endothelial cell proliferation, they are highly prone to invading the surrounding normal brain tissue, which is often one of the reasons for the failure of treatment. However, the mechanisms involved in this process are not fully understood. MicroRNAs (miRs) are a class of non‑coding RNA that are able to inhibit the malignant progression of tumor cells through the regulation of downstream genes. In the present study, the low expression of miR‑576‑3p was detected in glioma samples and hypoxia‑treated glioma cells using a reverse transcription‑quantitative polymerase chain reaction. The present study focused on the effects of miR‑576‑3p on hypoxia‑induced glioma. The results of the functional experiments revealed that the overexpression of miR‑576‑3p significantly inhibited the migration and pro‑angiogenic abilities of the glioma cells under hypoxic conditions (P

Importance Chronic subdural hematoma (CSDH) is a trauma-associated condition commonly found in elderly patients. Surgery is currently the treatment of choice, but it carries a significant risk of recurrence and death. Nonsurgical treatments remain limited and ineffective. Our recent studies suggest that atorvastatin reduces hematomas and improves the clinical outcomes of patients with CSDH. Objective To investigate the safety and therapeutic efficacy of atorvastatin to nonsurgically treat patients with CSDH. Design, Setting, and Participants The Effect of Atorvastatin on Chronic Subdural Hematoma (ATOCH) randomized, placebo-controlled, double-blind phase II clinical trial was conducted in multiple centers in China from February 2014 to November 2015. For this trial, we approached 254 patients with CSDH who received a diagnosis via a computed tomography scan; of these, 200 (78.7%) were enrolled because 23 patients (9.1%) refused to participate and 31 (12.2%) were disqualified. Interventions Patients were randomly assigned to receive either 20 mg of atorvastatin or placebo daily for 8 weeks and were followed up for an additional 16 weeks. Main Outcomes and Measures The primary outcome was change in hematoma volume (HV) by computed tomography after 8 weeks of treatment. The secondary outcomes included HV measured at the 4th, 12th, and 24th weeks and neurological function that was evaluated using the Markwalder grading scale/Glasgow Coma Scale and the Barthel Index at the 8th week. Results One hundred ninety-six patients received treatment (169 men [86.2%]; median [SD] age, 63.6 [14.2] years). The baseline HV and clinical presentations were similar between patients who were taking atorvastatin (98 [50%]) and the placebo (98 [50%]). After 8 weeks, the HV reduction in patients who were taking atorvastatin was 12.55 mL more than those taking the placebo (95% CI, 0.9-23.9 mL; P = .003). Forty-five patients (45.9%) who were taking atorvastatin significantly improved their neurological function, but only 28 (28.6%) who were taking the placebo did, resulting in an adjusted odds ratio of 1.957 for clinical improvements (95% CI, 1.07-3.58; P = .03). Eleven patients (11.2%) who were taking atorvastatin and 23 (23.5%) who were taking the placebo underwent surgery during the trial for an enlarging hematoma and/or a deteriorating clinical condition (hazard ratio, 0.47; 95% CI, 0.24-0.92; P = .03). No significant adverse events were reported. Conclusions and Relevance Atorvastatin may be a safe and efficacious nonsurgical alternative for treating patients with CSDH. Trial Registration ClinicalTrials.gov Identifier:NCT02024373

Jicai Zhang, Xiang Xiao, Jianming Zhu, Ziyun Gao, Xianliang Lai, Xingen Zhu, Guohua Mao Department of Neurosurgery, Second Affiliated Hospital, Nanchang University, Nanchang, Jiangxi, China Purpose: Glioblastoma multiforme (GBM) is the most common malignant brain tumor originating in the central nervous system in adults. Based on nanotechnology such as liposomes, polymeric nanoparticles, and lipid nanoparticles, recent research efforts have been aimed to target drugs to the brain. Methods: In this study, lactoferrin- and arginine–glycine–aspartic acid (RGD) dual-ligand-comodified, temozolomide and vincristine-coloaded nanostructured lipid carriers (L/R-T/V-NLCs) were introduced for GBM combination therapy. The physicochemical properties of L/R-T/V-NLCs such as particle size, zeta potential, and encapsulated efficiency are measured. The drug release profile, cellular uptake, cytotoxicity, tissue distribution, and antitumor activity of L/R-T/V-NLCs are further investigated in vitro and in vivo. Results: L/R-T/V-NLCs were stable with nanosize and high drug encapsulation efficiency. L/R-T/V-NLCs exhibited sustained-release behavior, high cellular uptake, high cytotoxicity and synergy effects, increased drug accumulation in the tumor tissue, and obvious tumor inhibition efficiency with low systemic toxicity. Conclusion: L/R-T/V-NLCs could be a promising drug delivery system for glioblastoma chemotherapy. Keywords: gliomatosis cerebri, combination therapy, nanostructured lipid carriers, lactoferrin, arginine–glycine–aspartic acid peptide, vincristine, temozolomide

Chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) is a steroid receptor that is broadly expressed in many tissues throughout embryonic development. Previous studies indicated that COUP-TFII is dysregulated in multiple types of cancer and serves crucial roles in cancer development. The mitochondrial pyruvate carrier 1 (MPC1) is involved in transporting pyruvate for entry into the citric acid cycle, an important event in cancer progression. However, the roles of COUP-TFII and MPC1 in glioma remain unknown. In the present study, it was demonstrated that MPC1 is downregulated in glioblastoma. Furthermore, the inhibition of COUP-TFII was able to increase MPC1 expression and inhibit the growth of glioblastoma cells in vitro and in vivo. The findings from the present study demonstrated that downregulation of COUP-TFII inhibits glioblastoma growth via targeting MPC1. Therefore, COUP-TFII is a potential therapeutic target for glioma.

Glioblastoma multiforme (GBM) is the most common malignant brain tumor originating in the central nervous system. Efficient delivery of therapeutic molecules to the cells and tissues is a difficult challenge.Arginine-glycine-aspartic acid peptide (RGD)-modified nanostructured lipid carriers (NLCs) were used for the delivery of temozolomide (TMZ) into the GBM to provide a new paradigm in gliomatosis cerebri treatment.RGD-conjugated polyethylene glycol-b-distearoylphosphatidylethanolamine (PEG-DSPE) was synthesized. RGD containing, TMZ-loaded NLCs (RGD-TMZ/NLCs) were prepared. Their particle size, zeta potential, drug encapsulation efficiency (EE) and drug release behavior were evaluated. In vitro cytotoxicity study of TMZ/NLCs was tested in U87 malignant glioma cells (U87MG cells). In vivo antitumor efficacy of the carriers was evaluated on mice bearing GBM model.The U87MG cells were successfully inhibited by RGD-TMZ/NLCs in vitro. RGD-TMZ/NLCs also displayed the highest antitumor efficacy in vivo than all the other formulations used for comparison.RGD-TMZ/NLCs were efficient in selective delivery of TMZ into U87MG cells, and inhibition efficacy is high. These RGD-modified vectors could be a superior drug delivery nano-system to achieve therapeutic efficacy, and this research could be a new promising strategy for treatment in malignant gliomatosis cerebri.

Co-delivery of gene and anticancer drug into the same cancer cells or tissues by multifunctional nanocarriers may provide a new paradigm in cancer treatment. In this study, nanostructured lipid carriers (NLCs) were constructed as multifunctional nanomedicine for co-delivery of enhanced green fluorescence protein plasmid (DNA) and temozolomide (TMZ).TMZ- and DNA-loaded NLCs (TMZ/DNA-NLCs) were prepared. Their particle size, zeta potential, gene-loading capacity (GL) and drug encapsulation efficiency (EE) were evaluated. In vitro cytotoxicity study TMZ/DNA-NLCs was tested in U87 malignant glioma cells (U87 MG cells). In vivo gene transfection and anti-tumor efficacy of the carriers were evaluated on mice bearing malignant glioma model.The optimum TMZ/DNA-NLCs formulations with the particle size of 179 nm and with a +23 mV surface charge; got 91% of GL and 83% of EE. The growth of U87 MG cells in vitro was obviously inhibited. TMZ/DNA-NLCs also displayed the highest gene transfection efficiency and the best antitumor activity than other formulations in vivo.The results demonstrated that TMZ/DNA-NLCs were efficient in selective delivery to malignant glioma cells. Also TMZ/DNA-NLCs transfer both drug and gene to the gliomatosis cerebri, enhance the antitumor capacity and gene transfection efficacy. Thus, TMZ/DNA-NLCs could prove to be a superior co-delivery nanomedicine to achieve therapeutic efficacy and this report could be a new promising strategy for treatment in malignant gliomatosis cerebri.

Growing number of long intergenic noncoding RNAs (lincRNAs) have recently been identified in mammals as new modulators in cancer origination and progression involved in a broad range of biological processes. Long intergenic noncoding RNA POU3F3 (linc-POU3F3) has been characterized as a highly conserved functional transcription regulator in esophageal squamous cell carcinoma. The contributions of this lincRNA to glioblastoma remain unknown. In this present study, we investigated the expression pattern and functional role of linc-POU3F3 in glioma by using real-time PCR and gain-/loss-of-function studies. The results revealed that linc-POU3F3 levels were extraordinarily associated with the tumor WHO grade. In related biochemical assays, overexpression of linc-POU3F3 promotes cell viability and proliferation in glioma cells, whereas knockdown of linc-POU3F3 showed the opposite effect. As expected, we also found that linc-POU3F3 expression was negatively correlated with the mRNA level of POU3F3 (the evolutionarily conserved neighbor gene of linc-POU3F3). Our results indicate that linc-POU3F3 might affect glioma development via altering expression level of POU3F3, and lead us to believe that linc-POU3F3 may also have a crucial regulatory role in glioma progression.

Mutations of isocitrate dehydrogenase 1 (IDH1) gene are most common in glioma, arguably preceding all known genetic alterations during tumor development. IDH1 mutations nearly invariably target the enzymatic active site Arg132, giving rise to the predominant IDH1R132H. Cells harboring IDH1 R132H -heterozygous mutation produce 2-hydroxyglutarate (2-HG), which results in histone and DNA hypermethylation. Although exogenous IDH1 R132H transduction has been shown to promote anchorage-independent growth, the biological role of IDH1R132H in glioma remains debatable. In this study, we demonstrate that heterozygous IDH1 R132H suppresses but hemizygous IDH1 R132H promotes anchorage-independent growth. Whereas genetic deletion of the wild-type allele in IDH1 R132H -heterozygous cells resulted in a pronounced increase in neurosphere genesis, restoration of IDH1 expression in IDH1 R132H -hemizygous cells led to the contrary. Conversely, anchorage-independent growth was antagonistic to the mutant IDH1 function by inhibiting gene expression and 2-HG production. Furthermore, we identified that in contrast to IDH1 R132H -hemizygous neurosphere, IDH1 R132H -heterozygous cells maintained a low level of reducing power to suppress neurosphere genesis, which could be bypassed, however, by the addition of reducing agent. Taken together, these results underscore the functional importance of IDH1 mutation heterozygosity in glioma biology and indicate functional loss of mutant IDH1 as an escape mechanism underlying glioma progression and the pathway of redox homeostasis as potential therapeutic targets.

Derived from brain glial cells, gliomas are currently the most common primary tumours in the central nervous system and are characterised by a high recurrence rate and poor prognosis. RWDD3 (RWD domain-containing sumoylation enhancer, also termed RSUME), which can be induced by cellular stress, such as CoCl2, heat shock and hypoxia, may play a crucial role in tumour angiogenesis, growth and metastasis. MicroRNAs (miRNAs) have been demonstrated to act as negative regulators of post-transcriptional gene expression and are involved in tumour growth and metastasis. In the present study, we explored the role of RWDD3 in glioma cell proliferation and invasion by the knockdown of RWDD3 with lentiviral shRNA and demonstrated that miRNA hsa-miR-375, regulates RWDD3 and has an important role in glioma progression. We found that expression of RWDD3 in high-grade gliomas was significantly higher than that noted in normal brain tissues and lower-grade gliomas in vivo. Knockdown of RWDD3 effectively led to cell cycle arrest, decreased proliferation and invasion, and increased apoptosis in human glioma cell lines. Furthermore, miR-375 was downregulated in human gliomas and overexpression of miR-375 caused downregulation of RWDD3 in glioma cells as well as inhibited their motility. Thus, these findings suggest that RWDD3 and miR-375 may function as therapeutic biomarkers for glioma patients.

Background Glioma is the most common cause of cancer-related death. Therapy based on radiation seemed to effectively, while the radioresistance of several glioblastoma cells abolished the therapy. Thus, to employ the potential mechanism underlying the radioresistance is essential for glioma treatment. Methods Radioresistant cells were constructed using the X-ray radiation. Cell viability and apoptosis were detect using CCK-8 and Annexin-V/propidium iodide (PI), respectively. Real-time PCR and western blot were performed to determine gene expression. Luciferase reporter assay was carried out to detect the relationship between miR-183 and LRIG1. Mice xenotransplant model of glioma was established to detect the role of miR-183 in vivo. Results The expression of miR-183 was increased, while LRIG1 was decreased in resistant tissues rather than in sensitive tissues. The expression of LRIG1 was lower in radioresistant gliblastoma cell line U251R rather than in normal glioblastoma cell line U251. Overexpressed miR-183 suppressed cell apoptosis in radioresistance U251R cells (U251R). MiR-183 targets LRIG1 to regulate its expression. U251R cells transfected miR-183 inhibitor promoted the expression of LRIG1, and decreased the expression of EFGR and p-Akt, while U251R cells co-transfected with shRNA-LRIG1 abolished the effects of miR-183 knockdown. U251 cells transfected with miR-183 mimic decreased the expression of LRIG1, and promoted the expression of EFGR and p-Akt, while cells co-transfected with pcDNA-LRIG1 abolished the effects of miR-183 overexpression. In vivo experiments demonstrated that miR-183 inhibitor suppressed tumor growth, while miR-183 mimic promoted tumor growth. Conclusion MiR-183 overexpression promoted radioresistance of glioblastoma via down-regulating LRIG1 and increasing the activity of EFGR/Akt.

Background It has been reported that Colon cancer-associated transcript 2 (CCAT2) is dysregulated in various cancers. We performed this meta-analysis to clarify its promising functions as a prognosis marker in malignant tumors. Methods Electronic databases, including PubMed, Medline, OVID, Cochrane Library, and Web of Science, were searched from inception to October 20, 2016. The hazard ratio (HR) and 95% confidence interval (CI) were calculated to explore the relationship between CCAT2 expression and survival, which were extracted from the eligible studies. The odds ratio (OR) was calculated to assess the association between CCAT2 expression and pathological parameters using RevMan5.3 software. Results Six original studies were included in this meta-analysis including 725 cancer patients. The pooled HR suggested that high CCAT2 expression was significantly correlated with overall survival (OS) (HR = 2.30, 95% CI: 1.62–3.25, p

Because long non-coding RNA ATB (activated by TGF-β) is dysregulated in many cancers, we performed a meta-analysis to determine its prognostic potential in malignant tumors.We searched electronic databases, including PubMed, Medline, OVID, Cochrane Library and Web of Science from inception until November 15, 2016 and identified eight studies with 818 cancer patients for the meta-analysis. We analyzed the hazard ratios (HRs) and 95% confidence intervals (CIs) to determine the relationship between lncRNA-ATB expression and overall survival (OS), recurrence -free survival (RFS), disease-free survival (DFS). We also use RevMan5.3 software to calculate odds ratio (ORs) to assess the association between lncRNA-ATB expression and pathological parameters including lymph node metastasis (LNM), distant metastasis (DM) and tumor stage.Our analysis showed that increased lncRNA-ATB expression was associated with OS (HR=2.82, 95% CI:1.98-4.00, P0.00001), DFS (HR=2.75, 95% CI:1.73-4.38, P0.0001), RFS(HR=3.96, 95% CI:2.30-6.81, P0.00001), LNM (OR=4.07, 95% CI 1.74-9.53, P=0.001), DM (OR=3.21, 95% CI 1.06-9.72, P=0.04) and high tumor stage (OR=2.81, 95% 1.78-4.43, P0.0001) in patients with other types of cancers that excluded pancreatic cancer.Meta-analysis demonstrated that increased lncRNA-ATB expression can be a useful prognostic biomarker in human cancer.

Glioma is a well‑known aggressive and malignant brain tumor, and accounts for ~30% of all brain and central nervous system tumors. A number of studies have indicated that the abnormal expression of specific microRNAs (miR) serves vital roles in the tumorigenesis and tumor development of human cancer, including glioma. miR‑216b has been studied in a number of types of cancer. However, the expression pattern, molecular function and underlying mechanisms of miR‑216b in glioma remain unclear. In the present study, it was demonstrated that the level of miR‑216b was significantly decreased in glioma tissues and cell lines compared with matched normal tissues and primary normal human astrocytes. The reduced miR‑216b expression level was correlated with the Karnofsky Performance Score and the World Health Organization grade of gliomas. Upregulation of miR‑216b repressed cell proliferation and invasion in glioma. Additionally, metadherin (MTDH) was identified as a direct target gene of miR‑216b in glioma. MTDH expression was demonstrated to be significantly upregulated and inversely associated with miR‑216b expression in glioma specimens. MTDH knockdowns could simulate the cellular conditions induced by miR‑216b overexpression in glioma cells. In addition, miR‑216b regulated phosphatidylinositol 3,4,5‑trisphosphate 3‑phosphatase and dual‑specificity protein phosphatase PTEN/protein kinase B signaling pathways in glioma. These results suggested that miR‑216b acted as a tumor suppressor in glioma by directly targeting MTDH and that the miR‑216b/MTDH axis may be an effective therapeutic target for the treatment of patients with this disease.

Glioma is the most common primary tumor in the central nervous system, characterized by rapid progression, aggressive behavior, frequent recurrence and poor prognosis. In the present study we demonstrated that chondroitin polymerizing factor (CHPF) is highly expressed in human glioma tissues and 4 glioma cell lines. To explore the role of CHPF in glioma, a lentiviral vector expressing CHPF shRNA was constructed and transfected into the glioma U251 cells, which stably downregulated the expression levels of the CHPF gene in U251 cells in vitro. U251 cell proliferation inhibition rates were determined by MTT assay. The effect of survivin shRNA on U251 cell cycle distribution and cell apoptosis was determined by flow cytometry. Compared to the shRNA‑Ctrl group of cells, the shRNA-CHPF group of cells exhibited decreased proliferation and a significant increase in the proportion of cells in the G0/G1 phase. In addition, we found that knockdown of the expression of CHPF increased apoptosis in glioma U251 cells. Therefore, our results confirmed that CHPF promotes growth and inhibits apoptosis in glioma U251 cells. Thus, by in vivo and in vitro data, the present study suggests that CHPF could be a new potential therapeutic target for glioma.

Objectives: To study the therapeutic effect and complications of deep brain stimulation (DBS) to Parkinson’s disease (PD). Patients and Methods: A retrospective analysis of DBS performed on 44 patients with Parkinson’s disease who had complications in the post-operation. Results: 1). A stimulation effect was observed in all PD patients during the operation, with the most obvious effect being relief of muscular tension, followed by improvement in tremor and bradykinesia. 2). The implantable pulse generator was activated from 3 days to 1 month after the implantation of the stimulation electrode, and then had an obvious effect. 3). Clinical follow-up was performed from 3 months to 2.5 years post-implantation. The symptoms assessed using the UPDRS score were significantly improved. 4). Two cases of cerebral hemorrhage and vesicular effusion were related to surgical methods. There were several cases of pneumonia in the postoperative fever and two cases of urinary system infection. One case of traverse fracture also occurred. Postoperative electrode exposure and local infection occurred in 1 case. There were 3 cases of lethargy, 2 cases of hallucinations. In the postoperative period, intelligence decreased further in 1 case. One patient had no obvious improvement in rigidity. 5). One case had difficulties in eye opening within 1 month. One case of PD had poor rigidity control. There was also decrease memory after stimulation in 2 cases. Conclusion: Proper selection of patients, appropriate DBS surgical methods and reasonable adjustment of stimulation parameters can effectively prevent and treat related complications.

Objective The aim of this study was to investigate the clinical efficacy of superficial temporal artery-middle cerebral artery anastomosis (STA-MCA) + encephalo-duro-myo-synangiosis (EDMS) in treating ischemic Moyamoya disease (IMD) in adults. Methods A total of 30 adult patients with IMD were selected to be included in the study; they underwent STA-MCA + EDMS and were followed up for 3 months to 2 years. The digital subtraction angiography findings, modified Rankin scale (mRs) score, and complications of all the patients were compared. Results Thirty patients successfully completed the surgery. Three patients had postoperative complications (two patients with cerebral infarction on the surgical side and one patient with poor scalp healing). The postoperative morbidity rate was 10%. Angiography conducted at 3 to 6 months postoperatively showed 28 cases of anastomotic patency; the anastomotic patency rate was 93.3%. The mRs scores of the patients’ neurological function 3 months after surgery were lower than those before surgery. Conclusion STA-MCA + EDMS is effective in treating Moyamoya disease.

BRAF activated non-coding RNA (BANCR) is often dysregulated in cancer. We performed a meta-analysis to clarify its functions as a prognostic indicator in malignant tumors. We searched the PubMed, Medline, OVID, Cochrane Library, and Web of Science databases to identify BANCR-related studies. Nine original studies and 898 total patients were included in the meta-analysis. Hazard ratios (HR) and 95% confidence intervals (CI) were extracted from the included studies to determine the relationship between BANCR expression and patient overall survival (OS). Odds ratios (OR) were calculated using RevMan 5.3 software to assess associations between BANCR expression and pathological parameters. High BANCR expression correlated with lymph node metastasis (LNM) (OR = 3.41, 95% CI: 1.82-6.37, P = 0.0001), distant metastasis (DM) (OR = 2.98, 95% CI: 1.76-5.07, P < 0.0001), tumor stage (OR = 3.11, 95% CI: 1.89-5.12, Z = 3.25, P < 0.0001), and poor OS (pooled HR = 1.98, 95% CI: 1.20-3.27, P = 0.008) in gastrointestinal (GI) cancer patients, but not in non-GI cancer patients. Our results support the notion that BANCR as a promising prognostic biomarker in Chinese patients with GI cancer.

Epigenetic alteration plays critical roles in gliomagenesis by regulating gene expression through modifications of Histones and DNA. Trimethylation of H3K9, an essential repressed transcription mark, and one of its methyltransferase, SUV39H1, are implicated in glioma pathogenesis and progression. We find that the protein level of HP1α, a reader of H3K9me3 is elevated in GOS3 and 1321N1 glioma cell lines. H3K9me3 and SUV39H1 level are also upregulated. Depletion of HP1α and SUV39H1 weakens GOS3 and 1321N1 cell proliferation capacity and results in apoptosis of cells. Furthermore, we find that HP1α and H3K9me3 are enriched in the FAS and PUMA promoters, which suggests that upregulated HP1α and H3K9me3 prevent apoptosis by suppressing apoptotic activators. These data indicates that up-regulated HP1α, SUV39H1, and H3K9me3 in glioma cells are functionally associated with glioma pathogenesis and progression, and may serve as novel biomarkers for future diagnostic and therapeutic targeting of brain tumors.

Ethnopharmacological relevance Hedyotis diffusa Willd (Rubiaceae) (HDW) has been widely applied for the treatment of tumors, inflammation and toxication in traditional Chinese medicine. The antitumor effect of HDW on glioblastoma has been rarely reported. We aim to evaluate the activity of this extract and explore the underlying mechanism in U87 human glioblastoma cell line. Materials and methods Cytotoxicity of HDW extract on U87 cells was measured by MTT assay. Apoptosis, cell cycle arrest and mitochondrial membrane potential (MMP) collapse induced by HDW extract were determined by flow cytometry. Caspase activity was analyzed based on colorimetric assay with a microplate spectrophotometer. Protein expression was examined by Western blot. Results HDW extract suppressed U87 cells growth in a dose- and time-dependent manner. Flow cytometry showed that HDW extract induced significant apoptosis, S/G2-M phase arrest and MMP collapse in U87 cells. Furthermore, dose-dependent activation of caspase-3, Bcl-2, Bax and ERK was observed with HDW extract treatment. Decreased Bcl-2/Bax ratio and Akt suppression were readily found as well. Conclusions Induction of mitochondria-mediated apoptosis played an essential role in antitumor activity of HDW extract in U87 cells, in which ERKs and Akt signaling proteins were also involved. These findings contributed to the feasibility of using HDW extract in glioblastoma treatment and the understanding of the molecular mechanism.

AIM To analyse the relationship between the Volume Embolization Ratio (VER), aneurysmal morphological characteristics, and intracranial aneurysm embolization results. MATERIAL AND METHODS Using the clinical and radiological data of 57 cerebral aneurysms treated with detachable coils, VERs were calculated. The relationship between the VER and aneurysm embolization was analysed. RESULTS We observed that the mean VERs of the small, medium, large, and giant aneurysms were 40.8±26.5%, 18.6±16.1%, 2.3±2.1% and 0.4±0.1%, respectively and the differences were statistically significant (F=7.091, P=0.000). The mean VERs of the wide- and small-necked aneurysms were 27.5±23.1% and 29.4±26.6%, respectively. There was no significant difference between these values. The mean VERs of aneurysms causing complete occlusion, neck residual and partial embolization were 41.8±29.3%, 31.4±21.2%, 12.3±15.1%, respectively, and the differences were statistically significant (F=7.97, p=0.001). CONCLUSION The VER is an objective index with which to evaluate aneurysm embolization and is a significant predictor of the efficacy of intracranial aneurysm embolization.