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. 2023 Jan 25;14(1):59. doi: 10.1038/s41419-023-05598-2

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© The Author(s) 2023

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. 5 — A Left, schematic diagram showing the process of circSLC38A1-pull down. The biotin-labeled probes were used to pull down interacting proteins in T24 cells, the pull-down proteins were identified by MS. Right, identification of the circSLC38A1-protein complex pulled down by circSLC38A1 probe with protein extracts from T24 cells. The arrows indicate the additional band presented in circSLC38A1-protein complex. B Immunoblot analysis of ILF3 after pulldown assay showing its specific association with circSLC38A1. C RIP assays showing the association of ILF3 with circSLC38A1 in T24 cells. Top, fold enrichment representing RNA levels associated with ILF3 relative to IgG, IgG antibody served as a control. Bottom, agarose gel electrophoresis for products of RIP assay. D Co-localization of circSLC38A1 and ILF3 visualized by coupling circRNA FISH assay with ILF3 Immunofluorescence staining; scale bar: 25 μm. E ILF3 is up-regulated in BC based on data available from TCGA database. F Relative expression of ILF3 in BC cell lines and human normal urothelial cell line detected by western blot. G Expression levels of ILF3 in BC and adjacent normal tissues were detected by immunohistochemical staining. H, I Interference with ILF3 can effectively reverse the migratory and invasive potential of bladder cancer cells induced by circSLC38A1. J The expression levels of E-cadherin, Vimentin, ILF3, and snail between pLCDH-circSLC38A1+si-NC and pLCDH-circSLC38A1 + siILF3^#1 group were detected by western blot. Data represent mean ± SD from three independent experiments; *P < 0.05, **P < 0.01, ***P < 0.001.