Research Paper Volume 9, Issue 8 pp 1885—1897

Epigenetic silencing of miR-338 facilitates glioblastoma progression by de-repressing the pyruvate kinase M2-β-catenin axis

Figure 3. MiR-338 expression inversely correlated with glioma malignancy and was restrained by CpG-island methylation. (A) Gene Ontology function analysis and KEGG pathway enrichment of miR-338-downregulated genes. (B) The expression difference of miR-338 between low-grade and high-grade gliomas in TCGA. (C) The methylation level of the miR-338 promoter region between low-grade and high-grade gliomas in TCGA. (D) Qrt-PCR of miR-338 expression 48 hours after cells were treated with dimethyl sulfoxide or 5-azacytidine (P<0.01 to 10nM 5aza, P<0.05 to 10nM 5aza). (E) Wound-healing assay; the scratch was photographed at 0 h, 24 h and 48 h after transfection. (F) Cell viability was examined with a CCK-8 assay at different time intervals after transfection (P<0.05, P<0.05, P<0.05, P<0.01, respectively). (G) Cellular ATP levels in SNB19 and LN229 glioma cell lines normalized with cell numbers 24 h, 48 h and 72 h post-transfection with miR-Scr or miR-338 (P<0.01).