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Glioblastoma is a highly aggressive disease with poor survival outcomes. An emerging body of literature links the role of the renin–angiotensin system (RAS), well-known for its function in the cardiovascular system, to the progression of cancers. We studied the expression of RAS-related genes (<i>ATP6AP2</i>, <i>AGTR1</i>, <i>AGTR2</i>, <i>ACE</i>, <i>AGT</i>, and <i>REN</i>) in The Cancer Genome Atlas (TCGA) glioblastoma cohort, their relationship to patient survival, and association with tumour microenvironment pathways. The expression of RAS genes was then examined in 12 patient-derived glioblastoma cell lines treated with chemoradiation. In cases of glioblastoma within the TCGA, <i>ATP6AP2</i>, <i>AGTR1</i>, <i>ACE</i>, and <i>AGT</i> had consistent expressions across samples, while <i>AGTR2</i> and <i>REN</i> were lowly expressed. High expression of <i>AGTR1</i> was independently associated with lower progression-free survival (PFS) (<i>p</i> = 0.01) and had a non-significant trend for overall survival (OS) after multivariate analysis (<i>p</i> = 0.095). The combined expression of RAS receptors (<i>ATP6AP2</i>, <i>AGTR1</i>, and <i>AGTR2</i>) was positively associated with gene pathways involved in hypoxia, microvasculature, stem cell plasticity, and the molecular characterisation of glioblastoma subtypes. In patient-derived glioblastoma cell lines, <i>ATP6AP2</i> and <i>AGTR1</i> were upregulated after chemoradiotherapy and correlated with an increase in <i>HIF1A</i> expression. This data suggests the RAS is correlated with changes in the tumour microenvironment and associated with glioblastoma survival outcomes.