Overexpression of RAB34 associates with tumor aggressiveness and immune infiltration in glioma
Abstract Background RAB34 is aberrantly expressed in various cancers and exhibits oncogenic properties. However, its function in glioma remains largely unclear. Herein, we investigated the clinical value and biological functions of RAB34 in glioma. Methods In this study, we collected 697 RNA-seq data from The Cancer Genome Atlas (TCGA) dataset and 325 RNA-seq data from Chinese Glioma Genome Atlas (CGGA) dataset. CCK-8 and EdU assays were employed to assess cell proliferation ability. The transwell assay was utilized to explore cell migration and invasion capacities. Western blot coupled with qRT-PCR were employed to determine the protein, as well as RNA contents. The statistical analyses along with the graphical work were mainly implemented in the R software. Results RAB34 expression was positively related to the glioma tumor grade, and predicted poor outcomes for glioma patients. RAB34 expression was significantly upregulated in classical and mesenchymal subtypes, and IDH wild-type gliomas. Additionally, RAB34 expression was regulated by promoter DNA methylation. Moreover, RAB34 expression was remarkably correlated with inflammatory activities, immune infiltration, and immune checkpoints in glioma. In vitro experiments demonstrated that inhibition of RAB34 restrained the growth, migration, as well as invasion of glioma cells, and reversed the epithelial-to-mesenchymal transition (EMT) process. Conclusion Our findings established RAB34 as a novel progression-related biomarker and a possible immunotherapy target for glioma.