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. 2023 Nov 23;21:846. doi: 10.1186/s12967-023-04730-2

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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 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. 5 — Effect of CFH knockdown on the function of RA FLS. RA FLSs were transfected with siRNAs for EIF3C (siEIF3C) or control siRNA (siCtrl) for 72 h and then stimulated with TNF-α(50 ng/ml) + CFH (5 μg/ml) for 24 h (n = 4–8). A Effect of EIF3C knockdown on the migration of RA FLSs was measured with the wound-healing assay. The relative migration rates were calculated by the percentage by which the original scratch area decreased and then normalized to that in the control group. B Effect of EIF3C knockdown on the invasion of RA FLSs using Transwell assay. The relative invasion rates were calculated by counting invaded cells and then normalized to that in the control group. Representative images (original magnification, × 200) are shown. C Effect of EIF3C knockdown on the inflammatory mediators of RA FLSs detected by ELISA. Data show the mean ± SEM. *p < 0.05; **p < 0.01