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. 2022 Aug 6;15:1549–1559. doi: 10.2147/CCID.S367347

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© 2022 Kuai and Jian.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

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A20 was the direct target of miR-23b-3p. (A) Schematic graph of binding sites between miR-23b-3p and TNFAIP3, and the evaluation of binding ability by dual luciferase reporter assay. The expression of A20 in miR-23b-3p inhibitor-transfected primary KFs (B), miR-23b-3p inhibitor-transfected KEL FIB cells (C), TGF-β1-treated primary KFs (D) and TGF-β1-treated KEL FIB cells (E). (F) The mRNA expression of A20 in keloid tissues. (G) The correlation between the expression of A20 and miR-23b-3p. ***P<0.001.

Abbreviation: mimics NC, negative control mimics.