Circ_CLIP2 promotes glioma progression through targeting the miR-195-5p/HMGB3 axis.

BACKGROUND: Circular RNA (circRNA) has been demonstrated to play key roles in regulating glioma progression. Understanding the regulatory mechanism of circRNA in glioma is vital to reveal the pathogenesis of glioma and develop novel therapeutic strategies. Therefore, our study focuses on the role and underlying mechanism of Circ_CLIP2 in glioma. METHODS: The expression of Circ_CLIP2, miR-195-5p and HMGB3 in glioma cells and tissues were analyzed using qRT-PCR. Cell proliferation was determined with colony formation and MTT assays. Cell cycle and apoptosis were examined by flow cytometry. Western blot was conducted for analyzing HMGB3, PCNA, Bax, Bcl-2, cleaved-caspase 3, Wnt-1 and ß-catenin. Dual-luciferase reporter assay was measured to investigate the interaction among Circ_CLIP2, miR-195-5p and HMGB3. RESULTS: The expression of Circ_CLIP2 and HMGB3 were increased while miR-195-5p was down-regulated in glioma cells and patients. Silencing of Circ_CLIP2 inhibited cell proliferation, enhanced cell apoptosis and inhibited the Wnt/ß-catenin signaling pathway. Circ_CLIP2 suppressed miR-195-5p expression by directly sponging miR-195-5p. MiR-195-5p inhibited HMGB3 expression via directly targeting HMGB3. Knockdown of miR-195-5p facilitated cell proliferation, inhibited cell apoptosis and activated Wnt/ß-catenin signaling, which were reversed by silencing of HMGB3. CONCLUSION: Knockdown of Circ_CLIP2 suppresses glioma progression by targeting miR-195-5p/HMGB3 thus inhibiting Wnt/ß-catenin signaling. This study may provide potential therapeutic targets against glioma.

A risk score based on admission characteristics to predict progressive hemorrhagic injury from traumatic brain injury in children.

Traumatic brain injury (TBI) is one of the leading causes of death and disability in children, and progressive hemorrhagic injury (PHI) post TBI is associated with poor outcomes. Therefore, the objective of this study was to develop and validate a prognostic model that uses the information available at admission to determine the likelihood of PHI occurrence after TBI in children. The identified demographic data, cause of injury, clinical predictors on admission, computed tomography scan characteristics, and routine laboratory parameters were collected and used to develop a PHI prognostic model with logistic regression analysis, and the prediction model was validated in 68 children. Eight independent prognostic factors were identified: lower Glasgow coma scale score (3 ~ 8) (6 points), intra-axial bleeding/brain contusion (4 points), midline shift ≥5 mm (9 points), platelets <100 × 109/L (11 points), prothrombin time >14 s (6 points), international normalized ratio >1.25 (7 points), D-dimer ≥5 mg/L (14 points), and glucose ≧10 mmol/L (11 points). We calculated risk scores for each child and defined three risk groups: low risk (0-16 points), intermediate risk (17-36 points), and high risk (37-68 points). In the development cohort, the PHI rates after TBI for the low-, intermediate-, and high-risk groups were 10.1, 47.9, and 84.2%, respectively. In the validation cohort, the corresponding PHI rates were 10.9, 47.5, and 85.4%, respectively. The C-statistic for the point system was 0.873 (p = 0.586 by the Hosmer-Lemeshow test) in the development cohort and 0.877 (p = 0.524 by the Hosmer-Lemeshow test) in the validation cohort. CONCLUSION: Using admission predictors, we developed a relatively simple risk score that accurately predicted the risk of PHI after TBI in children. What is Known: • TBI is one of the leading causes of death and disability in children, and PHI post TBI is associated with poor outcomes. •Prediction of patients at low risk of PHI could help reduce treatment costs, whereas identification of patients at high risk of PHI could direct early medical intervention to improve outcomes. What is New: • This study firstly developed a risk score system by assessing the admission information that could provide an earlier prediction of the occurrence of PHI after acute TBI in children.

Prediction of in-hospital recurrence and false-negative results in patients with COVID-19 by red blood cell values on admission.

The clinical characteristics and risk factors of patients with coronavirus disease 2019 (COVID-19) with re-positive or false-negative test results have so far remained to be determined. The present study provides a cross-sectional observational study on 134 hospitalized patients selected from Huoshenshan Hospital (Wuhan, China) using cluster sampling. A total of 68 patients had reduced red blood cell (RBC) counts, 55 a decrease in the hemoglobin concentration (HBC) and 73 a decline in hematocrit (HCT). The false-negative rate of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) RNA detection in pharyngeal swab specimens was 18.7%. The absolute lymphocyte count (ALC), RBC, HBC and HCT levels in false-negative patients were significantly higher than those in patients who tested positive for viral nucleic acids. Multivariate logistic regression analysis indicated that RBC [odds ratio (OR)=0.43, 95% CI: 0.18-0.99], HBC (OR=0.97, 95% CI: 0.94-0.99) and ALC (OR=0.43, 95% CI: 0.20-0.91) were the factors influencing the negative testing results for viral nucleic acid. The rate of re-positive patients was 16.4%. The white blood cell, RBC, HBC and HCT values in re-positive patients were lower than those in non-re-positive patients. The median (interquartile range) values for RBC, HBC and HCT of male re-positive patients were 3.95 (3.37, 4.2) x1012/l, 123 (103, 133) g/l and 36.6 (31.1, 39.2)%, respectively, while the RBC, HBC and HCT of female re-positive patients were 3.54 (3.13, 3.74) x1012/l, 115 (102, 118) g/l and 34.2 (28.5, 34.9)%, respectively. It was determined that RBC, HBC and HCT values had moderate accuracy in predicting SARS-CoV-2 recurrence in patients with COVID-19 using receiver operating curve analysis. The present study suggested that RBC may have an important role in the pathogenesis of COVID-19.

Laparoscopic transcystic common bile duct exploration in patients with a nondilated common bile duct.

BACKGROUND: Laparoscopic transcystic common bile duct exploration (LTCBDE) is the minimally traumatic surgical method for the treatment of choledocholithiasis secondary to cholecystolithiasis with dilated common bile duct (CBD). However, no report exists concerning LTCBDE in patients with nondilated CBD. The purpose of this study was thus to explore the safety, efficacy, and feasibility of LTCBDE in patients with choledocholithiasis secondary to cholecystolithiasis with nondilatation of the CBD. METHODS: We retrospectively analyzed 47 patients with choledocholithiasis secondary to cholecystolithiasis who were treated with LTCBDE at the Second Affiliated Hospital of Nanchang University from January 2017 to August 2021 (all the patients had undergone endoscopic retrograde cholangio-pancreatography treatment, but this failed due to various reasons). Clinical data on disease characteristics, methods for cystic duct incision and CBD stone extraction, and surgical outcomes were collected and reviewed. Each patient was followed up for more than 3 months. RESULTS: There were 47 patients in this study, including 21 females and 26 males, with their ages ranging from 15 to 82 years (51±15 years). All patients were treated with surgery, and the CBD stones were removed successfully. Among these patients, 45 underwent LTCBDE for the removal of stones in the CBD, with failure occurring in 2 patients who then accepted laparoscopic common bile duct stone removal (LCBDE) + T tube drainage. The diameter of the cystic duct was 0.30-0.73 cm (0.60±0.07 cm), the diameter of the CBD was 0.60-0.80 cm (0.73±0.05 cm), the operation time was 75-220 minutes (159±33 minutes), and the postoperative hospital stay was 2-13 days (6±2 days). None of the patients experience any serious postoperative complications, and all were discharged safely. During the follow-up, no postoperative biliary stenosis, bile leakage, or other complications occurred. CONCLUSIONS: LTCBDE is feasible to treat patients with choledocholithiasis secondary to cholecystolithiasis with nondilatation of the CBD. This choice of treatment plan reduces the length of hospital stay and the occurrence of postoperative complications. However, it is recommended that this be attempted on the basis of the experience of LTCBDE with dilated CBD.

Atorvastatin combined with dexamethasone in chronic subdural haematoma (ATOCH II): study protocol for a randomized controlled trial.

BACKGROUND: Chronic subdural haematoma (CSDH) is a common condition in the elderly that often requires neurosurgical management. For small CSDH, evidence has emerged that statins may reduce haematoma volume and improve outcomes, presumably by reducing local inflammation and promoting vascular repair. We wish to extend this evidence in a study that aims to determine the efficacy and safety of atorvastatin combined with low-dose dexamethasone in patients with CSDH. METHODS: The second ATorvastatin On Chronic subdural Hematoma (ATOCH-II) study is a multi-centre, randomized, placebo-controlled, double-blind trial which aims to enrol 240 adult patients with a conservative therapeutic indication for CSDH, randomly allocated to standard treatment with atorvastatin 20 mg combined with low-dose dexamethasone (or matching placebos) daily for 28 days, and with 152 days of follow-up. The primary outcome is a composite good outcome defined by any reduction from baseline in haematoma volume and survival free of surgery at 28 days. Secondary outcomes include functional outcome on the modified Rankin scale (mRS) and modified Barthel Index at 28 days, surgical transition and reduction in haematoma volumes at 14, 28 and 90 days. DISCUSSION: This multi-centre clinical trial aims to provide high-quality evidence on the efficacy and safety of the combined treatment of atorvastatin and low-dose dexamethasone to reduce inflammation and enhance angiogenesis in CSDH. TRIAL REGISTRATION: ChiCTR, ChiCTR1900021659 . Registered on 3 March 2019, http://www.chictr.org.cn/showproj.aspx?proj=36157 .

[Retracted] MicroRNA-375 inhibits glioma cell proliferation and migration by downregulating RWDD3 in vitro.

The authors of the above article drew to our attention that, in the above paper, 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 among the data panels, two pairs of panels in Fig. 4B were shown to be overlapping, and a further pair of panels showed overlapping data in Fig. 6B. The authors were presented with an opportunity to correct their figures in a Corrigendum, although it has subsequently come to light that the replacement figures themselves featured problems with overlapping data. Given the errors that have been identified in the compilation of the figures in this article, the Editor of Oncology Reports has decided that this article should be retracted from the publication owing to a lack of overall confidence in the presented data. The authors all agree to the retraction of this article, and the Editor and the authors apologize for any inconvenience that might result from this retraction. [the original article was published in Oncology Reports 39: 1825-1834, 2018; DOI: 10.3892/or.2018.6261].

Intravenous administration of human amniotic mesenchymal stem cells improves outcomes in rats with acute traumatic spinal cord injury.

We previously reported that intraspinal transplantation of human amniotic mesenchymal stem cells (hAMSCs) promotes functional recovery in a rat model of acute traumatic spinal cord injury (SCI). However, whether intravenous transplantation of hAMSCs also has therapeutic benefit remains uncertain. In this study, we assessed whether intravenous transplantation of hAMSCs improves outcomes in rats with acute traumatic SCI. In addition, the potential mechanisms underlying the possible benefits of this therapy were investigated. Adult female Sprague-Dawley rats were subjected to SCI using a weight drop device, and then hAMSCs or PBS were administered after 2 h via the tail vein. Our results indicated that transplanted hAMSCs could migrate to injured spinal cord lesion. Compared with the control group, hAMSCs transplantation significantly decreased the numbers of ED1 macrophages/microglia and caspase-3 cells, and reduced levels of inflammatory cytokines, such as tumor necrosis factor alpha, interleukin-6 and IL-1ß. In addition, hAMSCs transplantation significantly attenuated Evans blue extravasation, promoted angiogenesis and axonal regeneration. hAMSCs transplantation also significantly improved functional recovery. These results suggest that intravenous administration of hAMSCs provides neuroprotective effects in rats after acute SCI, and could be an alternative therapeutic approach for the treatment of acute SCI.

Non-coding RNAs: Regulators of glioma cell epithelial-mesenchymal transformation.

GBM (glioblastoma multiforme) is the most malignant form of glioma and is the most commonly occurring primary malignant brain tumour. GBM is difficult to completely excise, resulting in an extremely high recurrence rate. The occurrence of an aggressive glioma phenotype depends on EMT (epithelial-mesenchymal transformation), in which epithelial cells transform into mesenchymal cells by losing their cell-cell adhesion and polarity. NcRNAs (non-coding RNAs) play a significant role in the cellular progression from a normal phenotype to a cancerous phenotype. Recently, many studies have shown that there are two essential regulatory ncRNAs, miRNAs (microRNAs) and lncRNAs, which are closely related to EMT. In this review, we conducted a comprehensive investigation of the dysregulated lncRNAs and miRNAs in gliomas with particular attention to the function and regulatory mechanisms of several important lncRNAs and miRNAs, and we discussed their roles as glioma diagnostic and prognostic biomarkers and their potential clinical applications as therapeutic targets.

Mitochondria as Potential Targets and Initiators of the Blue Light Hazard to the Retina.

Commercially available white light-emitting diodes (LEDs) have an intense emission in the range of blue light, which has raised a range of public concerns about their potential risks as retinal hazards. Distinct from other visible light components, blue light is characterized by short wavelength, high energy, and strong penetration that can reach the retina with relatively little loss in damage potential. Mitochondria are abundant in retinal tissues, giving them relatively high access to blue light, and chromophores, which are enriched in the retina, have many mitochondria able to absorb blue light and induce photochemical effects. Therefore, excessive exposure of the retina to blue light tends to cause ROS accumulation and oxidative stress, which affect the structure and function of the retinal mitochondria and trigger mitochondria-involved death signaling pathways. In this review, we highlight the essential roles of mitochondria in blue light-induced photochemical damage and programmed cell death in the retina, indicate directions for future research and preventive targets in terms of the blue light hazard to the retina, and suggest applying LED devices in a rational way to prevent the blue light hazard.

Apc gene suppresses intracranial aneurysm formation and rupture through inhibiting the NF-κB signaling pathway mediated inflammatory response.

Background: Intracranial aneurysm (IA) is a critical acquired cerebrovascular disease that may cause subarachnoid hemorrhage, and nuclear factor-κB (NF-κB)-mediated inflammation is involved in the pathogenesis of IA. Adenomatous polyposis coli (Apc) gene is a tumor suppressor gene associated with both familial and sporadic cancer. Herein, the purpose of our study is to validate effect of Apc gene on IA formation and rupture by regulating the NF-κB signaling pathway mediated inflammatory response. Methods: We collected IA specimens (from incarceration of IA) and normal cerebral arteries (from surgery of traumatic brain injury) to examine expression of Apc and the NF-κB signaling pathway related factors (NF-κB p65 and IκBα). ELISA was used to determine levels of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß (IL-1ß), and IL-6. IA model was established in rats, and Apc-siRNA was treated to verify effect of Apc on IA formation and rupture. Next, regulation of Apc on the NF-κB signaling pathway was investigated. Results: Reduced expression of Apc and IκBα, and increased expression of NF-κB p65 were found in IA tissues. MCP-1, TNF-α, IL-1ß, and IL-6 exhibited higher levels in unruptured and ruptured IA, which suggested facilitated inflammatory responses. In addition, the IA rats injected with Apc-siRNA showed further enhanced activation of NF-κB signaling pathway, and up-regulated levels of MCP-1, TNF-α, IL-1ß, IL-6, MMP-2, and MMP-9 as well as extent of p65 phosphorylation in IA. Conclusion: Above all, Apc has the potential role to attenuate IA formation and rupture by inhibiting inflammatory response through repressing the activation of the NF-κB signaling pathway.

Knockdown of HOXC6 inhibits glioma cell proliferation and induces cell cycle arrest by targeting WIF-1 in vitro and vivo.

BACKGROUND: Homeobox C6 (HOXC6) is one of several HOXC genes and is frequently overexpressed in multiple cancers. However, the function and mechanism of HOXC6 in glioma remain unclear. METHODS: The expression level of HOXC6 and its relationship with prognosis in glioma were determined through the TCGA database. The expressions of HOXC6 mRNA in glioblastoma tissues and normal brain tissues were detected by qRT-PCR and Western blot. To explore the role of HOXC6 in glioma, a lentiviral vector that expressed HOXC6-shRNA was constructed and transfected into glioma U87 cells. The expression levels of HOXC6 and WNT inhibitory factor 1 (WIF-1) in the glioma U87 cells after transfection with HOXC6-shRNA were measured by real-time PCR and Western blot． CCK-8, colony formation and EdU assays were used to measure the effects of HOXC6 on U87 cell proliferation, and flow cytometry was used to monitor the changes in the cell cycle and cell apoptosis after transfection with HOXC6-shRNA. Xenograft tumors were examined in vivo for the carcinogenic effects and prognostic value of HOXC6 in glioma tissues. RESULTS: In this study, HOXC6 was highly expressed in human glioma tissues, and a high expression of HOXC6 was associated with poor prognosis in GBM patients. We demonstrated that HOXC6 was highly expressed in human GBM tissues and three glioma cell lines. The knockdown of HOXC6 expression significantly inhibited the proliferation and colony formation ability of U87 cells by blocking cell cycle progression in the G0/G1 phase and induced apoptosis. In addition, we found that the mRNA and protein levels of WIF-1 were substantially increased after transfection with HOXC6-shRNA compared with Ctrl-shRNA in vitro. Consistent with the results of the in vitro assays, the xenograft assay and immunohistochemistry also demonstrated that in response to HOXC6 inhibition, the tumor growth and Ki-67 expression level were inhibited and the WIF-1 expression was increased in vivo. CONCLUSIONS: In conclusion, the results of the current study indicate that HOXC6 promotes glioma U87 cell growth through the WIF-1/Wnt signaling pathway and HOXC6 might be a novel target in clinical treatment for gliomas.

Bioinformatics Analysis of Weighted Genes in Diabetic Retinopathy.

Purpose: Intricate signaling networks and transcriptional regulators translate pathogen recognition into defense responses. The aim of this study was to identify the weighted genes involved in diabetic retinopathy (DR) in different rodent models of diabetes. Methods: We performed a gene coexpression analysis of publicly available microarray data, namely, the GSE19122 dataset from the Gene Expression Omnibus database. We conducted gene coexpression analysis on the microarray data to identify modules of functionally related coexpressed genes that are differentially expressed in different rodent models. We leveraged a richly curated expression dataset and used weighted gene coexpression network analysis to construct an undirected network. We screened 30 genes in the most closely related module. A protein-protein interaction network was constructed for the genes in the most related module using the Search Tool for the Retrieval of Interacting Genes. Gene Ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis were performed for the 30 genes. Results: Five visual perception-related genes (Pde6g, Guca1a, Rho, Sag, and Prph2) were significantly upregulated. Based on the competing endogenous RNA hypothesis, a link between the long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and visual perception-related mRNAs was constructed using bioinformatics tools. Six potential microRNAs (miR-155-5p, miR-1a-3p, miR-122-5p, miR-223-3p, miR-125b-5p, and miR-124-3p) were also screened. Conclusions: MALAT1 might play important roles in DR by regulating Sag and Guca1a through miR-124-3p and regulating Pde6g through miR-125b-5p.

MicroRNA-375 inhibits glioma cell proliferation and migration by downregulating RWDD3 in vitro.

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.

Long noncoding RNA activated by TGF-ß in human cancers: A meta-analysis.

BACKGROUND: Because long non-coding RNA ATB (activated by TGF-ß) is dysregulated in many cancers, we performed a meta-analysis to determine its prognostic potential in malignant tumors. METHODS: 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. RESULTS: Our analysis showed that increased lncRNA-ATB expression was associated with OS (HR=2.82, 95% CI:1.98-4.00, P<0.00001), DFS (HR=2.75, 95% CI:1.73-4.38, P<0.0001), RFS(HR=3.96, 95% CI:2.30-6.81, P<0.00001), 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, P<0.0001) in patients with other types of cancers that excluded pancreatic cancer. CONCLUSIONS: Meta-analysis demonstrated that increased lncRNA-ATB expression can be a useful prognostic biomarker in human cancer.

Knockdown of linc-OIP5 inhibits proliferation and migration of glioma cells through down-regulation of YAP-NOTCH signaling pathway.

Long intergenic noncoding RNAs (lincRNAs) play important roles in regulating the biological functions and underlying molecular mechanisms of glioma. Here, we investigated the expression level and biological function of linc-OIP5 in glioma. In the current study, we used quantitative real-time polymerase chain reaction (qRT-PCR) to determine the expression of linc-OIP5 in glioma tissues and in adjacent normal tissues. Level of linc-OIP5 was up-regulated in glioma tissues and significantly correlated with the advanced tumor stage (III/IV). Subsequently, the efficacy of knockdown of linc-OIP5 by linc-OIP5-small interfering RNA (siRNA) was evaluated in vitro, and we found that knockdown of linc-OIP5 can inhibit glioma cells proliferation, migration in vitro and tumor formation in vivo. Further mechanistic studies revealed the effect of linc-OIP5 knockdown on glioma cell phenotype at least partially through down-regulation of YAP and inhibition of Notch signaling pathway activity. Thus, our study provides evidence that linc-OIP5 is a potential therapeutic target and novel molecular biomarker for glioma.

Lentivirus­mediated knockdown of chondroitin polymerizing factor inhibits glioma cell growth in vitro.

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 shRNA­Ctrl 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.

BRAF-activated lncRNA predicts gastrointestinal cancer patient prognosis: a meta-analysis.

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.

Long noncoding RNA CCAT2 can predict metastasis and poor prognosis: A meta-analysis.

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<0.00001) in cancer patients. Subgroup analysis revealed a significant association between CCAT2 and OS in urogenital system (HR=1.70, 95% CI: 1.27-2.26, p<0.003) and non-urogenital system cancer patients (HR=3.18, 95% CI: 2.09-4.83, p<0.0001). A significant association was observed between high CCAT2 expression and poor progression-free survival (PFS) in cancer patients (pooled HR=2.76, 95% CI: 1.74-4.37). CCAT2 expression was significantly related to lymph node metastasis (LNM) (OR=4.33, 95% CI 2.03-9.22), distant metastasis (DM) (OR=11.66, 95% CI: 5.36-25.37) and tumor stage (OR=2.58, 95% CI 1.86-3.57). CONCLUSIONS: This meta-analysis demonstrated that high CCAT2 expression significantly predicts poor OS, poor PFS, LNM, DM and tumor stage, suggesting that high CCAT2 expression may serve as a novel biomarker for poor prognosis and metastasis in cancers.

Long non-coding RNA HULC as a potential prognostic biomarker in human cancers: a meta-analysis.

Since the long non-coding RNA HULC (Highly Upregulated in Liver Cancer) 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 August 14, 2016 and identified seven studies with 730 cancer patients for the meta-analysis. We analyzed the hazard ratios (HRs) and 95% confidence intervals (CIs) to determine the relationship between HULC expression and overall survival (OS). We also using RevMan5.3 software to calculate odds ratio (ORs) to assess the association between HULC expression and pathological parameters, including lymph node metastasis (LNM), distant metastasis (DM) and the tumor stage. Our analysis showed that higher HULC expression was associated with OS (HR= 0.50, 95% CI: 0.35-0.70, P <0.00001), LNM (OR=0.20, 95 % CI 0.06-0.64), DM (OR=0.27, 95% CI: 0.13-0.54) and the tumor stage (OR=0.39, 95 % CI 0.25-0.64). These meta-analysis data demonstrate that higher HULC expression can be a useful prognostic biomarker in human cancers.

SNORD47, a box C/D snoRNA, suppresses tumorigenesis in glioblastoma.

SNORD47 is a member of the C/D box small nucleolar RNAs, which have been implicated in cancer development. We intended to investigate the therapeutic potential of SNORD47 in glioma. We found that the expression of SNORD47 was downregulated in glioma tissues samples and inversely associated with advanced tumor stage (WHO grade IV). Kaplan-Meier survival analysis revealed that glioma patients with high SNORD47 expression had longer overall survival than those with low SNORD47 expression. SNORD47 suppressed the proliferation of glioma cells and induced G2 phase arrest. In addition, upregulation of SNORD47 suppressed invasion and epithelial-mesenchymal transition in glioma cells, and combination treatment with lenti-SNORD47 could augment the anti-tumor effect of temozolomide. These results showed that SNORD47 acted as a tumor suppressor in glioma, and provided the potential anti-tumor function in glioma treatment.