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. 2017 Mar 22;11:84. doi: 10.3389/fncel.2017.00084

Figure 4.

Figure 4

Cyclin E2 (CCNE2) was up-regulated in glioma tissues. CCNE2 was a target of miR-370, both KCNQ1OT1 and miR-370 could modulate CCNE2 expression. (A) CCNE2 protein expression levels in normal brain tissues and glioma tissues using GAPDH as an endogenous control. Representative protein expression and their integrated light density values (IDVs) of CCNE2 in normal brain tissues, low-grade glioma tissues ([WHO] I-II), and high-grade glioma tissues ([WHO] III-IV) are shown. Data are presented as the mean ± SD (n = 5, each group). *P < 0.05 vs. NBTs group. (B) CCNE2 harbored a putative miR-370 binding site, and designed mutant sequences were indicated. (C) Dual-luciferase reporter assay of HEK 293T cells co-transfected with CCNE2-Wt and miR-370-NC or CCNE2-Wt and miR-370, and CCNE2-Mut and miR-370-NC or CCNE2-Mut and miR-370. Data are presented as the mean ± SD (n = 5, each group). *P < 0.05 vs. CCNE2-Wt + miR-370-NC group. (D) Western blot analysis for CCNE2 in KCNQ1OT1 knockdown of human glioma cells using GAPDH as an endogenous control. Data are presented as the mean ± SD (n = 5, each group). *P < 0.05 vs. sh-NC group. (E) Western blot analysis for CCNE2 in miR-370 over-expression and miR-370 inhibition of human glioma cells using GAPDH as an endogenous control. Data are presented as the mean ± SD (n = 5, each group). *P < 0.05 vs. pre-NC group; #P < 0.05 vs. anti-NC group. (F) Western blot analysis for CCNE2 in co-transfected KCNQ1OT1 inhibition with miR-370 over-expression or miR-370 inhibition of human glioma cells using GAPDH as an endogenous control. Data are presented as the mean ± SD (n = 5, each group). *P < 0.05 vs. sh-NC + pre-NC group.