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. 2018 Sep 24;22(12):5862–5876. doi: 10.1111/jcmm.13856

Figure 5.

Figure 5

MAPK1 was a target of miR‐217 and positively regulated by CRNDE in HCC cells. (A) The sequence of binding sites between MAPK1 and miR‐217, and the sequence of mutant MAPK1. (B) Dual luciferase reporter assays showed miR‐217 regulated the luciferase activity of MAPK1‐wt, rather than MAPK1‐mut in HCC cells. (C, D) Quantitative real‐time PCR and Western blot analysis revealed that miR‐217 inhibitors could significantly increase the expression of MAPK1 in HepG2 cells. MiR‐217 mimics could significantly decrease the expression of MAPK1 in Huh‐7 cells. (E, F) MiR‐217 restoration reduced the high expression of MAPK1 in CRNDE‐overexpressing HepG2 cells. MiR‐217 knockdown increased the low expression of MAPK1 in CRNDE‐knockout Huh‐7 cells. (G) Transfection efficiencies test verified by qRT‐PCR. (H) MAPK1 could not inversely regulate up‐stream CRNDE/miR‐217 expression in HCC cells. **P < 0.01, compared with NC group. ## P < 0.01, compared with CRNDE+miR‐217/sh‐CRNDE+anti‐miR‐217 group