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. 2018 Aug 30;9(9):888. doi: 10.1038/s41419-018-0882-5

Fig. 5. SNHG5 acts as a competing endogenous RNA and regulates GSK3β expression by competitively binding miR-26a-5p.

Fig. 5

a Luciferase reporter assay was applied to verify the targeted binding effect between SNHG5 3′UTR and miR-26a-5p. **P < 0.01. b Luciferase reporter assay was applied to verify the targeted binding effect between GSK3β 3′UTR and miR-26a-5p. **P < 0.01. c–e qRT-PCR analysis of SNHG5 and miR-26a-5p expression following transfected HepG2 and MHCC-97L cells with different regents. *P < 0.05, **P < 0.01. f The GSK3β mRNA levels after miR-26a-5p overexpression were deceted by qRT-PCR. **P < 0.01. g The GSK3β protein levels after miR-26a-5p overexpression or downregulation were deceted by western blot. h Pearson’s correlation analysis of the relationship between SNHG5 and miR-26a-5p expression levels in HCC tissues. i Western blot analyses of GSK3β expression after knockdown or upregulated SNHG5, while the inhibition of miR-26a-5p reversed the change in GSK3β expression