Objective: To analyze the expression of VMP1 in glioma and its relationship with prognosis of patients,and to explore its potential mechanism of action.Methods:1.VMP1 m RNA expression data and clinicopathological parameters of glioma patients in TCGA database,CGGA database and Gravendeel database were obtained for data analysis.The expression difference of VMP1 in glioma and normal brain tissue and the relationship between VMP1 and WHO grade and important molecular pathological subtypes of glioma were compared by U test and Oneway ANOVA.Kaplan-Meier survival analysis and Log-rank test were used to evaluate the difference in overall survival(OS)between the groups with high and low expression of VMP1.Univariate and multivariate Cox proportional risk regression models were used to determine the independent prognostic factors for patients with glioma.Based on the independent prognostic factors,a Nomogram model for predicting the survival rate of patients with glioma was constructed using CGGA data set as the training group to predict the survival rate of patients at 1,3 and 5 years.The TCGA and Gravendeel datasets were validated as external validation groups,and the prediction performance of the histogram was evaluated by C index,ROC curve and correction curve.Through TCGA database,According to |log FC|>1.5,P<0.05,the differentially expressed genes in the high and low expression groups of VMP1 were screened out And conducted GO enrichment analysis to explore its potential biological functions.2.The paraffin tissues of 63 glioma patients treated in the neurosurgery department of the Affiliated Tumor Hospital of Guangxi Medical University from January 2013 to December 2019 were collected and the expression of VMP1 protein was detected by immunohistochemical staining.To verify the expression of VMP1 in low-grade glioma(LGG)and high-grade glioma(HGG)tissues and its relationship with the prognosis of patients.Results: 1.The expression level of VMP1 m RNA in glioma tissue was significantly higher than that in normal brain tissue,and the difference was statistically significant(P<0.05).The expression of VMP1 in glioma increased with the increase of WHO grade,and the expression levels of VMP1 were significantly different among different grades(P<0.05).Compared with IDH mutant,the expression level of VMP1 m RNA in IDH wild-type glioma was significantly increased,and the difference was statistically significant(P<0.05).Multivariate Cox regression analysis showed that age,WHO grade and VMP1 expression were independent risk factors affecting overall survival(OS)of glioma patients.The C indexes of the CGGA training group,TCGA and Gravendeel validation group calculated by the nomogram model were 0.754,0.831 and 0.694,respectively;in the CGGA data set,the model predicted 1,3,and 5-year survival rates for the area under the ROC curve and the AUC values were 0.760,0.812 and 0.790,respectively.Gravendeel data set is 0.665,0.759 and 0.727 respectively,TCGA data set is 0.815,0.812 and 0.735 respectively.The calibration curve showed that the model predicted the results of each cohort had a high consistency with the actual observation results.A total of 933 differentially expressed genes were screened out in the high and low expression groups of VMP1 in TCGA,and GO enrichment analysis showed that VMP1 may be related to adhesion,migration and invasion ability of glioma cells.2.The expression of VMP1 in high-grade glioma was significantly higher than that in low-grade glioma(P < 0.001);The overall survival of glioma patients with high VMP1 expression was significantly shorter than that of glioma patients with low VMP1 expression(P=0.004).CONCLUSIONS: 1.VMP1 is highly expressed in glioma tissues,The higher the WHO grade,the higher its expression level;2.Age,WHO classification and VMP1 expression are independent risk factors affecting OS in glioma patients;3.Constructing a nomogram prediction model that integrates VMP1 expression and clinicopathological characteristics has good prediction performance;4.VMP1 may promote the occurrence and development of glioma by affecting the migration and invasion of glioma cells. |