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. 2020 Sep 15;19:1533033820959354. doi: 10.1177/1533033820959354

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© The Author(s) 2020

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 4. — MiR-92a interacted with SOX4 3’-UTR through the complementary sequences. (A) Wild type 3’-UTR of SOX4 contained the sequences for the interaction with miR-92a. Mutated 3’-UTR of SOX4 was constructed by the site-directed mutagenesis. (B) miR-92a overexpression in 293 T cells suppressed the luciferase activity of wild-type 3’-UTR of SOX4, with no obvious effect on that of mutated 3’-UTR of SOX4. (C) miR-92a knockdown in 293 T cells increased the luciferase activity of wild-type 3’-UTR of SOX4, with no obvious effect on that of mutated 3’-UTR of SOX4. *P < 0.05.