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. 2022 Feb 16;8:68. doi: 10.1038/s41420-022-00865-1

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© The Author(s) 2022

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 qRT-PCR for expression of circAFAP1 revealed that all the three siRNAs can reduce the expression in 786-O and A498 cells, while si-circAFAP1-3 displayed the most powerful silencing efficiency. ***represents p < 0.001. **represents p < 0.01. B, C CCK8 proliferation assays (B) and colony formation assays (C) displayed that the 786-O and A498 cells transfected with si-circAFAP1 have abrogated cell proliferation ability. ***represents p < 0.001. D Transwell assays were applied to discover the invasion ability after si-circAFAP1 transfection in 786-O and A498 cells. E Wound healing was applied to discover the migration ability after si-circAFAP1 transfection in 786-O and A498 cells. F Tube formation assay was applied to further validate the vascular promotion ability after adding the supernatant of si-circAFAP1 transfection of 786-O and A498 cells in HUVEC cells. G EdU assays were applied to further verify si-circAFAP1 inhibited the proliferation ability of 786-O and A498 cells.