Nuclear pore complex (NPC) is a major transport pivot for nucleocytoplasmic molecule exchange.
Nucleoporin 205 (NUP205)-a main component of NPC-plays a key regulatory role in
tumor cell proliferation; however, few reports document its effect on the pathological progression of lower-grade
glioma (LGG). Therefore, we conducted an integrated analysis using 906 samples from multiple public databases to explore the effects of NUP205 on the prognosis, clinicopathological characteristics, regulatory mechanism, and
tumor immune microenvironment (TIME) formation in LGG. First, multiple methods consistently showed that the
mRNA and
protein expression levels of NUP205 were higher in LGG
tumor tissue than in normal brain tissue. This increased expression was mainly noted in the higher WHO Grade, IDH-wild type, and 1p19q non-codeleted type. Second, various survival analysis methods showed that the highly expressed NUP205 was an independent risk
indicator that led to reduced survival time of patients with LGG. Third, GSEA analysis showed that NUP205 regulated the pathological progress of LGG via the cell cycle, notch signaling pathway, and aminoacyl-
tRNA biosynthesis. Ultimately, immune correlation analysis suggested that high NUP205 expression was positively correlated with the infiltration of multiple immune cells, particularly M2 macrophages, and was positively correlated with eight immune checkpoints, particularly PD-L1. Collectively, this study documented the pathogenicity of NUP205 in LGG for the first time, expanding our understanding of its molecular function. Furthermore, this study highlighted the potential value of NUP205 as a target of anti-LGG
immunotherapy.