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. 2023 Jul 6;14(7):404. doi: 10.1038/s41419-023-05919-5

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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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — A–D CCK-8 and Transwell assays showed the effect of DAGLA OE and KD on the proliferation and invasion ability of HCC cells treated with lenvatinib (10 μM). E Experimental scheme. F–I Xenograft tumours derived from DAGLA-knockdown cells and treated with lenvatinib (10 mg/kg) showed better tumour growth inhibition, while tumours derived from DAGLA-overexpressing cells showed significant lenvatinib resistance, which could be reversed by verteporfin (40 mg/kg). J, K Comparison of OS curves between 36 advanced recurrent HCC patients with high or low DAGLA and PHLDA2 levels treated with lenvatinib and TACE who underwent liver resection before combined therapy. L Schematic depiction of the mechanisms underlying the DAGLA/2-AG axis regulating HCC progression and lenvatinib resistance by enhancing YAP nuclear translocation and activity.