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. 2018 Aug 28;9(9):851. doi: 10.1038/s41419-018-0937-7

Fig. 4. DSCR8 functions as a sponge for miR-485-5p.

Fig. 4

a By applying bioinformatics tools (microRNA.org, TargetScan, and miRDB), we found that there were putative binding sites between 3′UTR of DSCR8-wild type (wt) and miR-485-5p. DSCR8-mutant (mut) means mutation of binding sites in the 3′UTR of DSCR8. b The expression of miR-485-5p in tumor tissues (n = 75) was significantly lower than that in adjacent non-tumor tissues (n = 75). c Pearson correlation analysis revealed that there existed a negative association between miR-485-5p and DSCR8 in HCC tissues. d MiR-485-5p was downregulated in HCC cell lines. e Real-time PCR showed that miR-485-5p was negatively regulated by DSCR8. f MiR-485-5p expression was significantly increased by miR-485-5p mimics, whereas decreased by the inhibitors. g The expression of DSCR8 was negatively regulated by DSCR8. h Luciferase reporter gene assays showed that miR-485-5p negatively regulated the luciferase activity of DSCR8-wt-3′UTR, rather than of DSCR8-mut-3′UTR. i The anti-Ago2 RIP assay with miR-485-5p mimics showed that both miR-485-5p and DSCR8 were enriched in Ago2 precipitate compared to IgG. n = three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001