Dual-specificity phosphatase 10 (DUSP10) correlates with
inflammation,
cytokine secretion, cell proliferation, survival, and apoptosis. However, its role in
glioma is unclear. Herein, we sought to examine the expression and the underlying carcinogenic mechanisms of DUSP10 action in
glioma. DUSP10 expression in
glioma was significantly higher than that in normal brain tissues. High DUSP10 expression indicated adverse clinical outcomes in
glioma patients. Increased DUSP10 expression correlated significantly with clinical features in
glioma. Univariate Cox analysis showed that high DUSP10 expression was a potential independent marker of poor prognosis in
glioma. Furthermore, DUSP10 expression in
glioma correlated negatively with its DNA methylation levels. DNA methylation level of DUSP10 also correlated negatively with poor prognosis in
glioma. More importantly, DUSP10 expression correlated positively with the infiltration of B cells, CD4+ T cells, CD8+ T cells, neutrophils, macrophages, and dendritic cells in
glioma. Gene set enrichment analysis (GSEA) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis confirmed that DUSP10 participated in signaling pathways involved in focal adhesion, TNF cascade, Th17 cell differentiation, and
NF-kappa B cascade. Finally, we uncovered that DUSP10 was dramatically upregulated in
glioblastoma (GBM) cells and that the knockdown of DUSP10 inhibited
glioma cell proliferation and migration. Our findings suggested that DUSP10 may serve as a potential prognostic
biomarker in
glioma.