MRC2 overexpression combined with intronic hypomethylation: potential predictors for glioma

Abstract

Purpose This study mainly to explore the effect of DNA methylation on the MRC2 expression, and the mechanism of MRC2 regulating the biological function of glioma cells. Methods MRC2 was found to be differentially expressed in glioma after large-scale screening of expression data. Logistic regression and Pearson correlation coefficient (r) scaled the correlation between MRC2 expression and clinical characteristics; immunohistochemistry and Western blot verified the expression of MRC2. ROC, Cox and Kaplan-Meier approach for quantifying MRC2 expression on survival. GSEA predicted signal pathways that may be activated by high expressed MRC2. Results High expression of MRC2 accompanied by promoter and intronic hypomethylation in glioma was related to survival rate, recurrence, tumor grade, chemotherapy, IDH_mutation, 1p19q_codeletion. Six pathways activated by highly expressed MRC2 were mainly regulated the proliferation and invasion in glioma. Co-expressed genes of MRC2 could be found in each pathway, and they were functionally consistent with MRC2. Conclusion The up-regulated MRC2 expression was related to promoter and intronic hypomethylation in glioma. Signal pathways activated by MRC2 mainly regulated the proliferation and invasion in glioma, and led to poor prognosis. MRC2 could be seen as a novel molecular target for glioma.