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. 2024 Nov 29;16:174. doi: 10.1186/s13148-024-01789-6

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 9 — Overexpression of THBS1 in PAX6-expressing HCC cells inhibited the antitumor function of PAX6. A We check the expression of THBS1 in HA22T cells transfected with THBS1 shRNAs (shTHBS1-1 and shTHBS1-2) or shCtrl via western blotting analysis. B Colony formation assays and C invasion assays were performed in HA22T cells. D We analyze the protein level of HA22T cells transfected with the specific combination of vectors, control vector, PAX6, or THBS1-V5. E AIG assays and F Matrigel invasion assays were employed to analyze the malignant phenotypes. The data are shown as the mean ± SE. We used the Mann‒Whitney U test to perform statistical analysis. * p < 0.05 and ** p < 0.01