Abstract
Epithelial membrane protein 3 (EMP3) is a tetraspan membrane protein overexpressed in isocitrate dehydrogenase-wild-type (IDH-wt) glioblastoma (GBM). Several studies reported high EMP3 levels as a poor prognostic factor in GBM patients. Experimental findings based on glioma and non-glioma models have demonstrated the role of EMP3 in the regulation of several membrane proteins known to drive IDH-wt GBM. In this review, we summarize what is currently known about EMP3 biology. We discuss the regulatory effects that EMP3 exerts on a variety of oncogenic receptors and discuss how these mechanisms may relate to IDH-wt GBM. Lastly, we enumerate the open questions towards EMP3 function in IDH-wt GBM.
Highlights
The diagnosis of glioblastoma (GBM) is applied to highly aggressive primary central nervous system (CNS) tumors
We summarized how the non-catalytic, multifunctional protein Epithelial membrane protein 3 (EMP3) is able to regulate the activity of several membrane receptors, most of which have been previously associated with isocitrate dehydrogenase (IDH)-wt GBM
EMP3 increases the activity of GBMrelevant receptor tyrosine kinase (RTK)
Summary
The diagnosis of glioblastoma (GBM) is applied to highly aggressive primary central nervous system (CNS) tumors. Three of the most common methylation subclasses among adult patients—RTK I, RTK II, MES—are enriched for the PN, CL, and MES Verhaak expression profiles, respectively [6] These tumor entities typically exhibit chromosome 7 gain (with or without epidermal growth factor receptor or EGFR amplification), as well as loss of chromosomes 9q21 and 10 [3,6,7]. Apart from genetic mutations, transcriptional alterations have been identified to be putative GBM contributors [5,6,9] These include the transcript coding for epithelial membrane protein 3 (EMP3), which is frequently overexpressed in IDH-wt GBM based on several studies [16,17,18,19]. We highlight its regulatory effects on several oncogenic membrane proteins and discuss how these mechanisms may contribute to the development of this dreaded disease
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