BRMS1 in Gliomas-An Expression Analysis

Simple Summary: Gliomas are the most common primary brain tumors and are associated with significant mortality and morbidity. Less than 5% of patients with glioblastoma, the most common glioma histology, survive longer than five years. Therefore, searching for new biomarkers/molecular targets remains a constant issue in glioma research. One such target may be the metastasis suppressor BRMS1. BRMS1 interacts with critical steps of the metastatic cascade in many cancer entities. However, due to the low incidence of extra-cerebral glioma metastasis, the role of metastasis-associated proteins in gliomas remains poorly investigated. Still, the changes in behavior modulated by BRMS1 across different entities (e.g., affecting invasion, migration, and apoptosis) closely resemble the changes seen in gliomas. Additionally, BRMS1's interaction partners are commonly dysregulated in gliomas. Therefore, BRMS1 shows potential as a regulator of glioma behavior, and we present the first insights into BRMS1 expression in gliomas as a starting point for further investigations. The metastatic suppressor BRMS1 interacts with critical steps of the metastatic cascade in many cancer entities. As gliomas rarely metastasize, BRMS1 has mainly been neglected in glioma research. However, its interaction partners, such as NF kappa B, VEGF, or MMPs, are old acquaintances in neurooncology. The steps regulated by BRMS1, such as invasion, migration, and apoptosis, are commonly dysregulated in gliomas. Therefore, BRMS1 shows potential as a regulator of glioma behavior. By bioinformatic analysis, in addition to our cohort of 118 specimens, we determined BRMS1 mRNA and protein expression as well as its correlation with the clinical course in astrocytomas IDH mutant, CNS WHO grade 2/3, and glioblastoma IDH wild-type, CNS WHO grade 4. Interestingly, we found BRMS1 protein expression to be significantly decreased in the aforementioned gliomas, while BRMS1 mRNA appeared to be overexpressed throughout. This dysregulation was independent of patients' characteristics or survival. The protein and mRNA expression differences cannot be finally explained at this stage. However, they suggest a post-transcriptional dysregulation that has been previously described in other cancer entities. Our analyses present the first data on BRMS1 expression in gliomas that can provide a starting point for further investigations.