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. 2019 May 23;18(1):489–496. doi: 10.3892/etm.2019.7603

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Copyright: © Zhao et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — Sp1 is the target gene of miR-202. (A) Schematic analysis of the possible binding site for miR-202 in the 3′UTR of Sp1. (B) Dual luciferase reporter assay showed that overexpression of miR-202 markedly suppressed the relative luciferase activity of pmirGLO-SP1-3′UTR in 293T cells. (C) The overexpression of miR-202 suppressed the protein level of Sp1 in SCC-9 cells. (D) Inhibition of miR-202 markedly enhanced the protein expression of Sp1 in SCC-9 cells. (E) Inhibition of miR-202 enhanced the phosphorylation of AKT in SCC-9 cells. n=3 independent experiments, *P<0.05, **P<0.01 and ***P<0.001 vs. control. p-Akt, phosphorylated protein kinase B; miR, microRNA; UTR, untranslated; si, small interfering; NC, negative control; NCm, negative control for miR-202 mimic; NCi, negative control for miR-202 inhibitor; RLU, relative luciferase units.