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. 2024 Sep 30;24:1211. doi: 10.1186/s12885-024-12973-5

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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. 8 — The influence of DYNLL1 on proliferation, apoptosis, migration and Wnt/β-catenin signalling pathway in HCC. (A) PCR was used to validate DYNLL1 knockdown in Huh7 and HepG2 cells. Pink represents si-1, blue represents si-2, dark green represents si-3, and light green represents si-4 group. (B) CCK-8 proliferation assays in Huh7 and HepG2 cell lines after DYNLL1 knockdown. (C) Apoptosis assay in Huh7 and HepG2 cell lines after DYNLL1 knockdown. (D) Wound healing assays in Huh7 and HepG2 cell lines after DYNLL1 knockdown. (E) Western blotting revealed changes in the expression levels of EMT-related proteins in HCC cells. (F) Western blotting revealed changes in the expression levels of proteins in the Wnt/β-catenin pathway. Pink represents si-DYNLL1,, and blue represents the siNC group. All the data are expressed as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.001; ns, not significant