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. 2020 Jul 29;11(7):594. doi: 10.1038/s41419-020-02784-4

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© The Author(s) 2020

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — amiR-141-3p and miR-200a-3p were overexpressed with miR-141-3p or miR-200a-3p mimics in Ishikawa cells, respectively, and be partly rescued by pHBLV-ATRNL1 co-transfection. mi-NC was taken as the control group. bmiR-141-3p and miR-200a-3p were downregulated with miR-141-3p or miR-200a-3p inhibitors in Ishikawa cells, respectively, and be partly rescued by sh1-circATRNL1 co-transfection. in-NC was taken as the control group. c–e CCK-8 and transwell assays were separately carried out to identify the influence of miR-141-3p and miR-200a-3p mimics on cell proliferation, migration, and invasion. Photographs were taken at ×200 magnification. Scale bar represents 100 μm. f The effect of miR-141-3p and miR-200a-3p mimics on EMT progress in Ishikawa cells was evaluated through detecting the EMT marker proteins with western blot analysis. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 represent statistical difference.