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. 2022 May 14;12:8007. doi: 10.1038/s41598-022-12076-w

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© The Author(s) 2022

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/.

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Establishment of lenvatinib-resistant cells. (A) Lenvatinib-resistant Hep3B cells were established by treatment with lenvatinib for > 2 months (LR7.5-3B). Immunoblotting analysis of phosphorylated ERK (p-ERK), ERK, and ACTB levels in Hep3B and LR7.5-3B cells with or without 3 μM lenvatinib for 4 h. (B) Huh6 and JHH-4 cells were treated with 1.875 and 7.5 μM lenvatinib, respectively, for > 1 month. After treatment of the above-mentioned Huh6 and JHH-4 cells with 3 µM lenvatinib for 4 h, phosphorylation levels of ERK (p-ERK), ERK and TUBB were analyzed by immunoblotting. The intensity with the internal control were indicated. (C,D) Cell proliferation was analyzed by Cell Counting Kit 8 (CCK-8) assays in normal (Hep3B) and lenvatinib-resistant (LR7.5-3B) Hep3B cells that had been treated with 3 μM lenvatinib at the indicated times (n = 4 per treatment). Three independent experiments of (A–D) were performed, and representative results are shown. *p < 0.05.