Protein arginine methyltransferase (PRMT8) in cancer: Genomic alterations, subcellular dynamics, and clinical implications.
TL;DR
Clinically, these PRMT8 alterations drive disease progression and therapy resistance, resulting in poor prognosis and reduced patient survival, underscore the need to incorporate PRMT8 alterations assessment in clinical practice to guide therapeutic decision-making and improve treatment outcomes in affected patient populations.
Abstract
PRMT8 encodes a protein arginine methyltransferase, which is primarily expressed in the brain and nervous system. Several studies have reported its alterations, which have been implicated in various cancers. However, the existing information remains unsystematic and fragmented due to inconsistency in methodology. This review aims to explore PRMT8 gene alterations in humans, their effects on cellular function and physiology, and their clinical implications. We conducted a narrative literature review covering all publications on PRMT8 alterations across different cancer types, their effect on tumour cell characteristics, and their impact on patient prognosis. Reported PRMT8 alterations include mutations, copy number amplifications, and single-nucleotide polymorphisms, which lead to overexpression or downregulation of PRMT8 protein in tumour cells. PRMT8 alterations compromise the efficacy of both chemotherapy and immune checkpoint inhibitor treatment. These alterations enable tumour cells to maintain pluripotency via activation of the PI3K/AKT/SOX2 signalling pathway, thereby promoting cellular proliferation, invasion, and colony formation. Clinically, these PRMT8 alterations drive disease progression and therapy resistance, resulting in poor prognosis and reduced patient survival. These findings underscore the need to incorporate PRMT8 alterations assessment in clinical practice to guide therapeutic decision-making and improve treatment outcomes in affected patient populations.