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Background  Glioblastoma is the most common adult primary brain tumor with near-universal fatality. Major histocompatibility complex (MHC) class I molecules are important mediators of CD8 activation and can be downregulated by cancer cells to escape immune surveillance. MR1 is a nonclassical MHC-I-like molecule responsible for the activation of a subset of T cells. Although high levels of MR1 expression should enhance cancer cell recognition, various tumors demonstrate MR1 overexpression with unknown implications. Here, we study the role of MR1 in glioma.    Methods  Using multi-omics data from the Cancer Genome Atlas (TCGA), we studied  MR1  expression patterns and its impact on survival for various solid tumors. In glioma specifically, we validated  MR1  expression by histology, elucidate transcriptomic profiles of  MR1  high versus low gliomas. To understand  MR1  expression, we analyzed the methylation status of the   MR1   gene and  MR1  gene-related transcription factor (TF) expression.    Results    MR1  is overexpressed in all grades of glioma and many other solid cancers. However, only in glioma,  MR1  overexpression correlated with poor overall survival and demonstrated global dysregulation of many immune-related genes in an  MR1 -dependent manner. MR1 overexpression correlated with decreased   MR1   gene methylation and upregulation of predicted  MR1  promoter binding TFs, implying  MR1  gene methylation might regulate MR1 expression in glioma.    Conclusions  Our in silico analysis shows that  MR1  expression is a predictor of clinical outcome in glioma patients and is potentially regulated at the epigenetic level, resulting in immune-related genes dysregulation. These findings need to be validated using independent in vitro and in vivo functional studies.

MR1 overexpression correlates with poor clinical prognosis in glioma patients