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. 2024 Oct 9;43:280. doi: 10.1186/s13046-024-03203-8

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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. 8 — A working model explaining how hepatocyte-derived Igκ promotes HCC progression by stabilizing ETFA to facilitate fatty acid β-oxidation. Hepatocyte-derived Vκ4-1/Jκ3-Igκ interacts with the electron transporter ETFA on the mitochondrial respiratory chain, and loss of Igκ promotes ETFA protein degradation, leading to decreased expression of mitochondrial respiratory chain complexes III and IV, thereby causing aberrant FAO and lipid accumulation. Dysregulated lipid metabolism subsequently inhibits the proliferation and migration of HCC cells, thereby delaying HCC development