Expression of neuropilin-1 is linked to glioma associated microglia and macrophages and correlates with unfavorable prognosis in high grade gliomas
Metrics: PDF 1161 views | HTML 1430 views | ?
Michael D. Caponegro1, Richard A. Moffitt2,3 and Stella E. Tsirka1
1Program in Molecular and Cellular Pharmacology, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, USA
2Department of Biomedical Informatics, Stony Brook University, Stony Brook, NY, USA
3Department of Pathology, Stony Brook University, Stony Brook, NY, USA
Stella E. Tsirka, email: Stylianifirstname.lastname@example.org
Keywords: neuropilin; GAM; TCGA; glioma; glioblastoma
Received: July 29, 2018 Accepted: October 16, 2018 Published: November 02, 2018
High grade gliomas, including glioblastoma (GB), are devastating malignancies with very poor prognosis. Over the course of the last decade, there has been a failure to develop new treatments for GB. Reasons for this failure include the lack of validation of novel molecular targets, which are often characterized in animal models and directly transposed to human trials. Here we build on our previous findings, which describe how the multi-functional co-receptor Neuropilin-1 (NRP1) signals through glioma associated microglia/macrophages (GAMS) to promote murine glioma, and investigate NRP1 expression in human glioma. Clinical and gene expression data were obtained via The Cancer Genome Atlas (TCGA), and analyzed using R statistical software. Additionally, CIBERSORT in silico deconvolution was used to determine fractions of immune cell sub-populations within the gene expression datasets. We find that NRP1 expression is correlated with poor prognosis, glioma grade, and associates with the mesenchymal GB subtype. In human GB, NRP1 expression is highly correlated with markers of monocytes/macrophages, as well as genes that contribute to the pro-tumorigenic phenotype of these cells.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.