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. 2021 Feb 17;21(4):297. doi: 10.3892/ol.2021.12558

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Copyright: © Wang 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 5. — FAM83A-AS1 functions as competing endogenous RNA to regulate FAM83A by sponging miR-495-3p. (A) Expression of FAM83A-AS1 positively correlated with the expression of FAM83A in LUAD. (B) Knockdown of FAM83A-AS1 downregulated the expression of FAM83A. (C) Predicted using LncBase and StarBase, miR-495-3p could interact with both FAM83A-AS1 and FAM83A. (D and E) miR-495-3p mimics significantly reduced the expression of FAM83A-AS1 and FAM83A. (F) Potential binding sites of miR-495-3p with FAM83A-AS1 and FAM83A. (G) WT and MUT FAM83A-AS1/FAM83A sequences were constructed according to the putative binding sites. (H and I) miR-495-3p decreased the luciferase activity of wild-type FAM83A-AS1 and FAM83A reporter plasmids. ***P<0.001 miRNA/miR, microRNA; NC, negative control; WT, wild-type; MUT, mutant.