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. 2020 Jul 27;11(7):593. doi: 10.1038/s41419-020-2726-3

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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. 2 — a The morphologic changes in A549 and PC9 cells overexpressing circASPH were observed using a scanning electron microscopy assay. b, c DNA synthesis assessed using an EdU assay in the lenti-circASPH cells and control cells. Nuclei were stained with Hoechst 33342 (blue). The quantified data are presented as the percentage of EdU-incorporated cells. Log2 transformation was applied to deal with the ratio results and to obtain the normally distributed data. Then, T test was used to compare the difference between groups. d, e The migration of A549 and PC9 cells was significantly increased by circASPH overexpression. The migration distances (μm) of A549 and PC9 cells were quantified. f, g The invasion of A549 and PC9 cells was apparently increased by circASPH overexpression. The quantified data are presented as the number of invading cells per HPF. HPF high-power field. h–j Xenograft tumor models show that tumors grown from the circASPH-overexpressing cells were bigger than those grown from the control cells. k Western blot analysis of the levels of HMGA2 protein in the xenograft tumors. l IHC staining of the HMGA2 protein in the xenograft tumors. Every cell test was carried out in triplicate, and n = 3 for each cell group.