Glycine Receptor Beta Subunit (GlyR-ß) Promotes Potential Angiogenesis and Neurological Regeneration during Early-Stage Recovery after Cerebral Ischemia Stroke/Reperfusion in Mice.

BACKGROUND: Ischemic stroke is mainly caused by cerebral artery thrombosis. This study investigated the role of glycine receptor beta subunit (GlyR-ß) in the recovery from cerebral ischemia stroke/reperfusion. METHODS: The oxygen glucose deprivation and recovery (OGD/R) bEnd3 cell model and the middle cerebral artery occlusion/reperfusion (MCAO/R) mouse model were used in this study. RESULTS: Expression of both the GlyR-ß gene and vascular endothelial growth factor (Vegf), cell proliferation, and tube formation ability was decreased in bEnd3 cells after OGD/R, and was reversed by overexpression of GlyR-ß. Neurological function, asindicated by Zea Longa scores, area of cerebral ischemia, and pathological changes were increased in mice after MCAO/R, and were ameliorated by overexpression of the glycine receptor beta (Glrb) gene at 24 h and 7 d after MCAO/R. Expression of GlyR-ß and Gap-43 was decreased, and the expression of CD34, Vegf, and Bdnf, and cell growth as determined by a bromodeoxyuridine (BrdU) assay, increased in the affected brain tissue of MCAO/R mice in a time-dependent manner. GlyR-ß overexpression resulted in enhanced expression of CD34, Vegf, Growth association protein 43 (Gap-43), and brain-derived neurotrophic factor (Bdnf) and cell growth in affected brain tissue of MCAO/R mice in a time-dependent manner. CONCLUSIONS: GlyR-ß promoted potential angiogenesis and neurological regeneration in affected brain tissue, thus promoting recovery from cerebral ischemia stroke/reperfusion.

An inflammation-associated ferroptosis signature optimizes the diagnosis, prognosis evaluation and immunotherapy options in hepatocellular carcinoma.

Inflammation and ferroptosis crosstalk complexly with immune microenvironment of hepatocellular carcinoma (HCC), thus affecting the efficacy of immunotherapy. Herein, our aim was to identify the inflammation-associated ferroptosis (IAF) biomarkers for contributing HCC. A total of 224 intersecting DEGs identified from different inflammation- and ferroptosis-subtypes were set as IAF genes. Seven of them including ADH4, APOA5, CFHR3, CXCL8, FTCD, G6PD and PON1 were used for construction of a risk model which classified HCC patients into two groups (high and low risk). HCC patients in the high-risk group exhibited shorter survival rate and higher immune score, and were predicted to have higher respond rate in immune checkpoint inhibition (ICI) therapy. Levels of the seven genes were significantly changed in HCC tissues in comparison to adjacent tissues. After inserting the gene expression into the risk model, we found that the risk model exhibited the higher diagnostic value for distinguish HCC tissues compared each single gene. Furthermore, HCC tissues from our research group with high-risk score exhibited more cases of microsatellite instability (MSI), heavier tumour mutational burden (TMB), higher expression level of PDL1 and cells with CD8. Knockdown of APOA5 reduced HCC cell proliferation combining with elevating inflammation and ferroptosis levels. In conclusion, we considered APOA5 maybe a novel target for suppressing HCC via simultaneously elevating inflammation and ferroptosis levels, and signature constructed by seven IAF genes including ADH4, APOA5, CFHR3, CXCL8, FTCD, G6PD and PON1 can act as a biomarker for optimising the diagnosis, prognosis evaluation and immunotherapy options in HCC patients.

NCOA3 identified as a new candidate to explain autosomal dominant progressive hearing loss.

Hearing loss is a frequent sensory impairment in humans and genetic factors account for an elevated fraction of the cases. We have investigated a large family of five generations, with 15 reported individuals presenting non-syndromic, sensorineural, bilateral and progressive hearing loss, segregating as an autosomal dominant condition. Linkage analysis, using SNP-array and selected microsatellites, identified a region of near 13 cM in chromosome 20 as the best candidate to harbour the causative mutation. After exome sequencing and filtering of variants, only one predicted deleterious variant in the NCOA3 gene (NM_181659, c.2810C > G; p.Ser937Cys) fit in with our linkage data. RT-PCR, immunostaining and in situ hybridization showed expression of ncoa3 in the inner ear of mice and zebrafish. We generated a stable homozygous zebrafish mutant line using the CRISPR/Cas9 system. ncoa3-/- did not display any major morphological abnormalities in the ear, however, anterior macular hair cells showed altered orientation. Surprisingly, chondrocytes forming the ear cartilage showed abnormal behaviour in ncoa3-/-, detaching from their location, invading the ear canal and blocking the cristae. Adult mutants displayed accumulation of denser material wrapping the otoliths of ncoa3-/- and increased bone mineral density. Altered zebrafish swimming behaviour corroborates a potential role of ncoa3 in hearing loss. In conclusion, we identified a potential candidate gene to explain hereditary hearing loss, and our functional analyses suggest subtle and abnormal skeletal behaviour as mechanisms involved in the pathogenesis of progressive sensory function impairment.

Dominating lengthscales of zebrafish collective behaviour.

Collective behaviour in living systems is observed across many scales, from bacteria to insects, to fish shoals. Zebrafish have emerged as a model system amenable to laboratory study. Here we report a three-dimensional study of the collective dynamics of fifty zebrafish. We observed the emergence of collective behaviour changing between ordered to randomised, upon adaptation to new environmental conditions. We quantify the spatial and temporal correlation functions of the fish and identify two length scales, the persistence length and the nearest neighbour distance, that capture the essence of the behavioural changes. The ratio of the two length scales correlates robustly with the polarisation of collective motion that we explain with a reductionist model of self-propelled particles with alignment interactions.

Building an Immune-Related Genes Model to Predict Treatment, Extracellular Matrix, and Prognosis of Head and Neck Squamous Cell Carcinoma.

Due to the considerable heterogeneity of head and neck squamous cell carcinoma (HNSCC), individuals with comparable TNM stages who receive the same treatment strategy have varying prognostic outcomes. In HNSCC, immunotherapy is developing quickly and has shown effective. We want to develop an immune-related gene (IRG) prognostic model to forecast the prognosis and response to immunotherapy of patients. In order to analyze differential expression in normal and malignant tissues, we first identified IRGs that were differently expressed. Weighted gene coexpression network analysis (WGCNA) was used to identify modules that were highly related, and univariate and multivariate Cox regression analyses were also used to create a predictive model for IRGs that included nine IRGs. WGCNA identified the four most noteworthy related modules. Patients in the model's low-risk category had a better chance of survival. The IRGs prognostic model was also proved to be an independent prognostic predictor, and the model was also substantially linked with a number of clinical characteristics. The low-risk group was associated with immune-related pathways, a low incidence of gene mutation, a high level of M1 macrophage infiltration, regulatory T cells, CD8 T cells, and B cells, active immunity, and larger benefits from immune checkpoint inhibitors (ICIs) therapy. The high-risk group, on the other hand, had suppressive immunity, high levels of NK and CD4 T-cell infiltration, high gene mutation rates, and decreased benefits from ICI therapy. As a result of our research, a predictive model for IRGs that can reliably predict a patient's prognosis and their response to both conventional and immunotherapy has been created.

Multi-Hazard Effects of Crosswinds on Cascading Failures of Conventional and Interspersed Railway Tracks Exposed to Ballast Washaway and Moving Train Loads.

The interspersed railway track is an enhanced timber railway track, spot-replacing damaged wooden sleepers with new concrete sleepers to improve the bearing capacity of existing railway lines. Although this interspersed solution is characterised by low cost and short maintenance time, the interspersed tracks have worse stability than concrete tracks and can deteriorate quickly when exposed to extreme weather conditions such as heavy rains and floods. In many cases, heavy rains and floods are accompanied by strong winds. Ballast washaway can often be observed under flood conditions while the mass of trains is unevenly distributed on two rails due to the effect of lateral wind load and rail irregularities. The current work is the first in the world to investigate the collective multi-hazard effects of ballast washway and uneven axle loads on the vulnerability of conventional and interspersed railway tracks using nonlinear FEM software, STRAND 7. The train bogie is modelled by two sets of point loads. The maximum displacement, bending moment and twists have been studied to evaluate the worst condition. The novel insights will help the railway industry develop proper operations of interspersed railway tracks against naturally hazardous conditions.

Dual-Path Information Fusion and Twin Attention-Driven Global Modeling for Solar Irradiance Prediction.

Accurate prediction of solar irradiance holds significant value for renewable energy usage and power grid management. However, traditional forecasting methods often overlook the time dependence of solar irradiance sequences and the varying importance of different influencing factors. To address this issue, this study proposes a dual-path information fusion and twin attention-driven solar irradiance forecasting model. The proposed framework comprises three components: a residual attention temporal convolution block (RACB), a dual-path information fusion module (DIFM), and a twin self-attention module (TSAM). These components collectively enhance the performance of multi-step solar irradiance forecasting. First, the RACB is designed to enable the network to adaptively learn important features while suppressing irrelevant ones. Second, the DIFM is implemented to reinforce the model's robustness against input data variations and integrate multi-scale features. Lastly, the TSAM is introduced to extract long-term temporal dependencies from the sequence and facilitate multi-step prediction. In the solar irradiance forecasting experiments, the proposed model is compared with six benchmark models across four datasets. In the one-step predictions, the average performance metrics RMSE, MAE, and MAPE of the four datasets decreased within the ranges of 0.463-2.390 W/m2, 0.439-2.005 W/m2, and 1.3-9.2%, respectively. Additionally, the average R2 value across the four datasets increased by 0.008 to 0.059. The experimental results indicate that the model proposed in this study exhibits enhanced accuracy and robustness in predictive performance, making it a reliable alternative for solar irradiance forecasting.

Fault Diagnosis of Wind Turbine Generators Based on Stacking Integration Algorithm and Adaptive Threshold.

Fault alarm time lag is one of the difficulties in fault diagnosis of wind turbine generators (WTGs), and the existing methods are insufficient to achieve accurate and rapid fault diagnosis of WTGs, and the operation and maintenance costs of WTGs are too high. To invent a new method for fast and accurate fault diagnosis of WTGs, this study constructs a stacking integration model based on the machine learning algorithms light gradient boosting machine (LightGBM), extreme gradient boosting (XGBoost), and stochastic gradient descent regressor (SGDRegressor) using publicly available datasets from Energias De Portugal (EDP). This model is automatically tuned for hyperparameters during training using Bayesian tuning, and the coefficient of determination (R2) and root mean square error (RMSE) were used to evaluate the model to determine its applicability and accuracy. The fitted residuals of the test set were calculated, the Pauta criterion (3σ) and the temporal sliding window were applied, and a final adaptive threshold method for accurate fault diagnosis and alarming was created. The model validation results show that the adaptive threshold method proposed in this study is better than the fixed threshold for diagnosis, and the alarm times for the GENERATOR fault type, GENERATOR_BEARING fault type, and TRANSFORMER fault type are 1.5 h, 5.8 h, and 3 h earlier, respectively.

FUT11 is a target gene of HIF1α that promotes the progression of hepatocellular carcinoma.

Hypoxia promotes the progression of hepatocellular carcinoma. However, the hypoxia regulatory network in hepatocellular carcinoma is known to be limited. Thus, this study aimed to identify the crucial hypoxia-associated genes and to explore their effects and molecular mechanisms in hepatocellular carcinoma cells. FUT11 was first identified as a crucial hypoxia-associated gene through bioinformatics analysis. High FUT11 mRNA levels were positively correlated with poor clinical parameters. FUT11 knockdown under normoxia and hypoxia both decreased hepatocellular carcinoma cell proliferation, colony formation, migration, and invasion. HIF1α binds to the promoter of FUT11 and increases its transcription and co-expression with FUT11 in hepatocellular carcinoma tissues. Overexpression of FUT11 in HIF1α knockdown cells reversed the inhibitory effects of HIF1α suppression on hepatocellular carcinoma cell proliferation and mobility under hypoxia. Therefore, our findings indicate that FUT11 is a key target gene of HIF1α, which can promote the proliferation and mobility of hepatocellular carcinoma cells. FUT11 may be a novel and effective target for blocking the hypoxia response of hepatocellular carcinoma cells.

Preparing for the Improving Medicare Post-Acute Care Transformation Act: Incorporating A Sociotechnical Perspective to Enhance a Health Information Technology Evaluation Framework Applied to Post-Acute Care.

The Improving Medicare Post-Acute Care Transformation Act, which mandates electronic sharing of standardized patient data by post-acute care clinical settings, will likely spur further health information technology adoption and evaluation. To support evaluation, the study objective was to clarify components of an evidence-based health information technology evaluation framework, Health Information Technology Reference-based Evaluation Framework, by using the framework in home healthcare and incorporating a sociotechnical perspective in the health information technology evaluation. With 36 observations among three diverse home healthcare agencies, researchers conducted a recorded think-aloud process as nurses documented the home healthcare admission in the EHR. Thematic analysis revealed 15 themes that provided clarification for almost one-third of Health Information Technology Reference-based Evaluation Framework components and added a new concept. All themes reflected a sociotechnical perspective. The new theme added to the Health Information Technology Reference-based Evaluation Framework reflected the sociotechnical perspective: routine use. We anticipate the enhanced Health Information Technology Reference-based Evaluation Framework to be used by evaluators from diverse disciplines, to further facilitate context-dependent health information technology adoption in post-acute care settings.

Impact of Home Care Admission Nurses' Goals on Electronic Health Record Documentation Strategies at the Point of Care.

Home care nurses have multiple goals at the patient admission visit. Electronic health records support some of these goals, including high-quality documentation, but nurses may not complete the electronic documentation at the point of care. To characterize admission nurses' practices at the point of care and lay the foundation for design recommendations, this study investigates admission nurses' documentation strategies with respect to entering electronic data and how nursing goals affect them. We conducted 10 observations of home care agency admissions with five admission nurses in rural Pennsylvania. We collected screenshots and recorded the admission process. We asked the nurses questions outside the point of care. We coded the nurses' strategies at the data-entry screen level. Using thematic analysis, we investigated the influence of nursing goals on documentation strategies. Subject matter experts reviewed our findings. Several goals affect nurses' documentation strategies: ensure data accuracy, reduce time in the patient's home, and prevent infection. Home care admission nurses distribute the electronic documentation temporally due to their goals. Nurses developed memory aids to support completion of the documentation after leaving the patients' homes. Design and training should support the distributed manner in which home care nurses document patient encounters.

A Human Factors Engineering Study of the Medication Delivery Process during an Anesthetic: Self-filled Syringes versus Prefilled Syringes.

BACKGROUND: Prefilled syringes (PFS) have been recommended by the Anesthesia Patient Safety Foundation. However, aspects in PFS systems compared with self-filled syringes (SFS) systems have never been explored. The aim of this study is to compare system vulnerabilities (SVs) in the two systems and understand the impact of PFS on medication safety and efficiency in the context of anesthesiology medication delivery in operating rooms. METHODS: This study is primarily qualitative research, with a quantitative portion. A work system analysis was conducted to analyze the complicated anesthesia work system using human factors principles and identify SVs. Anesthesia providers were shadowed: (1) during general surgery cases (n = 8) exclusively using SFS and (2) during general surgery cases (n = 9) using all commercially available PFS. A proactive risk assessment focus group was followed to understand the risk of each identified SV. RESULTS: PFS are superior to SFS in terms of the simplified work processes and the reduced number and associated risk of SVs. Eight SVs were found in the PFS system versus 21 in the SFS system. An SV example with high risk in the SFS system was a medication might need to be "drawn-up during surgery while completing other requests simultaneously." This SV added cognitive complexity during anesthesiology medication delivery. However, it did not exist in the PFS system. CONCLUSIONS: The inclusion of PFS into anesthesiology medication delivery has the potential to improve system safety and work efficiency. However, there were still opportunities for further improvement by addressing the remaining SVs and newly introduced complexity.

Dynamical order and many-body correlations in zebrafish show that three is a crowd.

Zebrafish constitute a convenient laboratory-based biological system for studying collective behavior. It is possible to interpret a group of zebrafish as a system of interacting agents and to apply methods developed for the analysis of systems of active and even passive particles. Here, we consider the effect of group size. We focus on two- and many-body spatial correlations and dynamical order parameters to investigate the multistate behavior. For geometric reasons, the smallest group of fish which can exhibit this multistate behavior consisting of schooling, milling and swarming is three. We find that states exhibited by groups of three fish are similar to those of much larger groups, indicating that there is nothing more than a gradual change in weighting between the different states as the system size changes. Remarkably, when we consider small groups of fish sampled from a larger group, we find very little difference in the occupancy of the state with respect to isolated groups, nor is there much change in the spatial correlations between the fish. This indicates that fish interact predominantly with their nearest neighbors, perceiving the rest of the group as a fluctuating background. Therefore, the behavior of a crowd of fish is already apparent in groups of three fish.

Case report: Pulmonary sarcomatoid carcinoma demonstrating rapid growth on follow-up CT.

Background: The tumor growth rate and tumor volume doubling time are crucial parameters in diagnosing and managing lung lesions. Pulmonary sarcomatoid carcinoma (PSC) is a unique and highly malignant subtype of lung cancer, with limited documentation on its growth feature. This article aims to address the gap in knowledge regarding a PSC's growth patterns by describing the characteristics of a confirmed case using computed tomography, thereby enhancing the understanding of this rare disease. Case presentation: A 79-year-old man was transferred to our center presenting with a mild cough, blood-tinged sputum, and a malignant nodule in the left upper lobe. Chest CT revealed a solid nodule in the left upper lobe. A follow-up CT ten days later showed a significant increase in the size of the nodule, accompanied by ground-glass opacity in the surrounding lung. The rapid preoperative growth of the nodule suggested a non-neoplastic lesion, and intraoperative frozen pathology also considered the possibility of tuberculosis. Subsequently, a left upper apical-posterior segment (S1 + 2) resection was performed. Postoperative tumor pathology confirmed the diagnosis of pulmonary sarcomatoid carcinoma with extensive giant cell carcinoma and necrosis. Immunohistochemistry indicated approximately 60% PD-L1 positive and genetic testing revealed a MET mutation. The patient was discharged with oral crizotinib targeted therapy, and his condition remained stable postoperatively. The patient is currently undergoing regular follow-up at our hospital, with no evidence of distant metastasis or recurrence. Conclusion: Pulmonary sarcomatoid carcinoma can exhibit rapid tumor growth on imaging, and PSC should be considered in the differential diagnosis for lesions that present with a fast growth rate. Timely and appropriate treatment for PSC may lead to a good prognosis.

Expression, Prognostic Value, and Biological Function of CTHRC1 in Different Types of Gliomas: A Bioinformatic Analysis and Experiment Validation.

Background: In recent years, abnormal expression of collagen triple helix repeat containing 1 (CTHRC1) has been found in some tumors, closely related to the poor prognosis of cancer patients. However, the clinical significance of CTHRC1 in gliomas is not completely understood. Methods: We investigated the expression, prognostic value, and potential biological function of CTHRC1 in different types of gliomas through bioinformatics analysis and experimental verification. Results: Bioinformatics analysis revealed several key findings regarding the expression and clinical significance of CTHRC1 in gliomas. First, the analysis demonstrated a positive correlation between CTHRC1 expression and the World Health Organization (WHO) grading of gliomas, a relationship that was validated through immunohistochemistry experiments. In addition, a trend was observed in which CTHRC1 expression increased with the extent of glioma invasion, as supported by Western blot experiments. Subsequent bioinformatics analysis identified the mesenchymal subtype of gliomas as having the highest levels of CTHRC1 expression, a finding reinforced by immunohistochemical staining. Moreover, high CTHRC1 expression was associated with poor prognosis in gliomas and emerged as an independent prognostic factor, with varying impacts on prognosis between low-grade gliomas (LGGs) and glioblastoma (GBM) subgroups. Notably, comparative analysis unveiled distinct patterns of immune infiltration of CTHRC1 in LGG and GBM. Furthermore, alterations in copy number variations and DNA methylation were identified as potential mechanisms underlying elevated CTHRC1 levels in gliomas. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that CTHRC1 and its associated genes mainly function in the extracellular matrix and participate in tumor-related signaling pathways. Conclusions: The CTHRC1 has shown significant clinical utility as a prognostic marker and mesenchymal subtype marker of glioma.

Understanding the Information Needs of Pharmacy Staff Using CancelRx: A Qualitative Study of the Use of Prescription E-cancellation.

Background: Although electronic prescription cancellation such as via CancelRx can facilitate critical communication between prescribers and pharmacy staff about discontinued medications, there is little work that explores whether CancelRx meets the needs of pharmacy staff users. Objective: This study leverages qualitative interviews with pharmacy staff to address the following question: When medication changes are made by a prescriber using CancelRx, what information is needed by pharmacy staff to make correct and effective decisions in their roles in medication management? Methods: We conducted an inductive thematic analysis of interviews with 11 pharmacy staff members (pharmacists and pharmacy technicians) across three outpatient community pharmacy sites within an academic health care system. Results: Three information needs themes were consistently identified by both pharmacists and pharmacy technicians: prescriber intent when initiating the CancelRx, clinical rationale for the medication change, and intended medication regimen. Notably, both pharmacists and pharmacy technicians often reported seeking multiple information needs not fully addressed by CancelRx in the electronic health record (EHR) to achieve the shared goals of correct dispensing of medications and supporting patient self-management. Conclusions: Our qualitative analysis reveals that outpatient community pharmacy staff in an academic health care system often seek additional information from the (EHR) following medication changes communicated by CancelRx to meet their information needs. Ideally, the prescriber would provide sufficient information through CancelRx to automatically identify all discontinued prescriptions. These limitations highlight the need for design features that support routine communication of needed information at the time of a medication change, such as structured data elements.

EphB3 receptor suppressor invasion, migration and proliferation in glioma by inhibiting EGFR-PI3K/AKT signaling pathway.

Eph receptors are the largest subfamily of receptor tyrosine kinases, and they have been shown to play a crucial role in glioma. The EphB3 receptor is a member of this family, and its effect on the invasion, migration and proliferation of glioma cells was examined in this study. It was found that the expression of EphB3 was decreased in glioma specimens with increasing tumor grade. Additionally, the U87MG and U251 cell lines showed low levels of EphB3 expression. This finding was consistent with the negative correlation between EphB3 expression in glioma tissues and tumor grade. Depletion of EphB3 gene in U87MG and U251 cell lines resulted in a substantial enhancement of their invasion, migration, and proliferation capacities in vitro. Furthermore, the knockdown of EphB3 led to an upregulation of EGFR, p-PI3K, and p-AKT protein levels. On the other hand, EphB3 overexpression reduced the invasiveness, proliferative capacity and migration rate of U87MG and U251 cells, and downregulated EGFR, p-PI3K and p-AKT. These findings indicate that EphB3 functions as a tumor suppressor in glioma, and its downregulation enhances the malignant potential of glioma cells by activating the EGFR-PI3K/AKT pathway. Thus, EphB3 is a promising diagnostic marker for glioma, and the EphB3-EGFR-PI3K / AKT axis deserves further investigation as a potential therapeutic target.

Knockdown of FUT11 inhibits the progression of gastric cancer via the PI3K/AKT pathway.

Gastric cancer (GC) is a common and highly malignant tumor of the digestive tract. Members of the focused fucosyltransferase (FUT) family participate in the advancement of various types of cancer. However, research of FUT family members in the progression of GC known to be limited. The purpose of the research was to determine the function of important affiliates of the FUT family in GC and to explore its impacts on the proliferation and migration of GC cells and molecular mechanisms. For the study, fucosyltransferase11 (FUT11) was confirmed to be the only affiliate of the FUT family that was upmodulated in GC tissues and linked to poor survival according to GEPIA data. Furthermore, compared with adjacent noncancerous tissues, the expression of FUT11 was increased in GC tissues. The elevated FUT11 expression suggested that the overall survival (OS) rate of GC is low. Inhibition of FUT11 significantly reduced the proliferation and migration and suppressed the PI3K/AKT pathway by down-regulated collagen type VI alpha 3 chain (COL6A3) in GC cells. The present study has demonstrated that reinstating the expression of COL6A3 in gastric cancer (GC) cells can counteract the inhibitory impact of FUT11 knockdown on the proliferation and migration of GC cells. In conclusion, FUT11 may serve as a novel biomarker for GC, as it modulates GC cell proliferation and migration through the PI3K/AKT signaling pathway.

GOLPH3 Promotes Vasculogenic Mimicry via the Epithelial Mesenchymal Transition in Glioblastoma Cells.

AIM: To evaluate the relationship between Golgi phosphoprotein 3 (GOLPH3) and vasculogenic mimicry (VM) in glioblastoma cells. MATERIAL AND METHODS: Glioma tissues from 40 glioma patients with different pathological grades were collected. GOLPH3 and VM were evaluated by immunostaining in glioma tissues. Then, the correlation between GOLPH3 and VM were analyzed clinically. Additionally, a GOLPH3-downregulation lentivirus was constructed and transfected into the human primary glioblastoma cell line, U-87 MG. Afterwards, apoptosis, migration and invasion were assessed to determine the effects of downregulation GOLPH3. Then, E-cadherin and matrix metalloproteinase 2 (MMP2) were detected for assessment of the epithelial mesenchymal transition (EMT). RESULTS: GOLPH3 and VM were found to be positively correlated following clinical analysis (p < 0.01, r=0.788). Furthermore, GOLPH3 downregulation suppressed the migration and invasion of U87 MG cells (p < 0.05), followed by upregulation of E-cadherin and downregulation of MMP2. CONCLUSION: Collectively, our results demonstrate that GOLPH3 promoted VM in glioblastoma cells and that the corresponding mechanism was associated with the EMT. Our finding suggests that GOLPH3 may represent a promising therapeutic target for mitigating the recurrence and invasion of gliomas.