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. 2021 Feb 6;16:116. doi: 10.1186/s13018-021-02248-1

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — TNFAIP3 is a target of miR-143-3p and could be indirectly regulated by HAND2-AS1. a The potential binding sites of miR-143-3p on TNFAIP3 3′ UTR. b, c The interaction between miR-143-3p and TNFAIP3 was verified using dual-luciferase reporter and RIP assays. d Western blot analysis of TNFAIP3 expression in MH7A cells transfected with miR-143-3p or miR-NC. e Western blot analysis of TNFAIP3 expression in MH7A cells transfected with vector + miR-NC, HAND2-AS1 + miR-NC, or HAND2-AS1 + miR-143-3p. f, g qRT-PCR and Western blot analysis of TNFAIP3 expression in RA synovial tissues and normal synovial tissues. h, i Pearson correlation analysis of TNFAIP3 and miR-143-3p or HAND2-AS1 expression in 28 RA tissues. **P < 0.001, ***P < 0.0001