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. 2024 May 3;24:557. doi: 10.1186/s12885-024-12313-7

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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. 5 — FGL1 drives invasion and migration through IMPDH1 in ESCC cells. (A-C) Quantification of IMPDH1 expression levels in FGL1-OE TE1 cells transfected with IMPDH1 shRNA (sh-IMPDH1) or random nonsense sequences (sh-NC) using qRT-PCR (A) and western blotting (B and C). β-Actin served as the loading control. (D) The effects of IMPDH1 knockdown on FGL1-OE TE1 cells invasion were evaluated by transwell invasion assay. Scale bars, 100 μm. (E) The effects of FGL1 knockdown on FGL1-OE TE1 cells migration were evaluated by wound healing assay. Scale bars, 100 μm. The statistical difference was assessed with the two-tailed unpaired Student t test in A, C, D and E. Error bars show the SD from three independent experiments. ***p < 0.001, ****p < 0.0001