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. 2020 Aug 5;20:372. doi: 10.1186/s12935-020-01471-w

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© The Author(s) 2020

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. 5 — ACTA2-AS1 modulated the expression of SMAD3 by repressing miR-143-3p. a The mRNA levels of SMAD3 in CC tissues were tested using qRT-PCR. b The mRNA expression of SMAD3 in cervical cancer cell lines was examined. c, d The mRNA and protein expression levels of SMAD3 were determined after transfecting miR‐143‐3p mimic and inhibitor. e, f. The mRNA and protein expressions of SMAD3 were tested after silencing ACTA2‐AS1. g The mRNA expression of SMAD3 was detected after transfected with si-NC, si-ACTA2-AS1, si-ACTA2-AS1 + miR-143-3p inhibitor and si-ACTA2-AS1 + inhibitor NC, respectively. GAPDH was used as an internal control. *P < 0.05; ** P < 0.01