Resumen
The mesenchymal (MES) phenotype of glioblastoma (GBM) confers resistance to various therapeutic strategies and results from both tumor-intrinsic genetic alterations and tumor-extrinsic microenvironmental factors. In this study, we sought to identify and validate the key genes that regulate the MES phenotype of glioma via both mechanisms. By integrating bulk tumor data (using the TCGA and CGGA databases) and single-cell sequencing data of GBM, we revealed that the plasminogen activator, urokinase receptor (PLAUR) is the hub gene of the protumor microenvironment, encompassing hypoxia and immunosuppression, and we elucidated its role in driving the MES transition through both tumor-intrinsic function and cell-to-cell interaction. Our findings indicate that PLAUR may be a potential target for GBM treatment, as our research elucidated its functions through a comprehensive study.