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. 2024 May 30;22:517. doi: 10.1186/s12967-024-05233-4

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© The Author(s) 2024

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 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. 7 — CircDCAF8 promoted HCC progression through the miR-217/NAP1L1 axis. A, B Colony formation and EdU assays evaluated the proliferation ability in LV-circDCAF8 Hep-3B cells and LV-circDCAF8 Hep-3B cells transfected with miR-217 mimics or sh-NAP1L1 vectors. Scale bar = 50 μm. C Transwell assay measured invasion and migration ability with or without matrix. Scale bar = 500 μm. D Wound healing assay determined cell migration ability. Scale bar = 100 μm. E, F Immunofluorescence and western blot detected the expression of NAP1L1 and EMT-related proteins. Scale bar = 50 μm. Data are representative of three independent experiments and are presented as means ± SDs. (*p < 0.05; **p < 0.01; ***p < 0.001)