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. 2017 Aug 2;9(8):1885–1897. doi: 10.18632/aging.101271

Figure 3. MiR‐338 expression inversely correlated with glioma malignancy and was restrained by CpG‐island methylation.

Figure 3

(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).