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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. 6 — The effect of ACTA2-AS1/miR-143-3p/SMAD3 axis on progression of CC. a The knock-down ability of si-SMAD3 in HeLa and SiHa cells was confirmed by qRT-PCR. b The over-expression ability of pcDNA-ACTA2-AS1 was confirmed by qRT-PCR. c Cell viability was detected by CCK8 assay after transfecting with si-SMAD3 and co-transfecting with pcDNA‐ACTA2‐AS1 or miR-143-3p inhibitor. d The migration ability of transfected cells was analyzed by transwell assay. e Apoptosis condition of transfected cells was analyzed by flow cytometry analysis. ** P < 0.01, *P < 0.05