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Elevated expression of immunoglobulin (Ig), especially the Ig\u03ba free light chain with a unique V\u03ba4-1\/J\u03ba3 rearrangement in cancer cells, is linked to increased malignancy and has been implicated in colon cancer tumorigenesis. However, the role of Ig\u03ba in HCC carcinogenesis remains unclear. The aim of this study was to elucidate the pivotal roles of hepatocyte-derived Ig\u03ba in HCC development.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The rearrangement sequence and expression level of hepatocyte-derived Ig\u03ba in HCC cells were determined via RT-PCR, Sanger sequencing, immunohistochemistry, and western blot analysis. The function of Ig\u03ba in HCC tumorigenesis was assessed by silencing Ig\u03ba using siRNA or gRNA in various HCC cell lines. To assess the role of Ig\u03ba in HCC pathogenesis in vivo, a mouse model with hepatocyte-specific Ig\u03ba knockout and diethylnitrosamine (DEN) and carbon tetrachloride (CCL4)-induced HCC was utilized. The molecular mechanism by which Ig\u03ba affects HCC tumorigenesis was investigated through multiomics analyses, quantitative real-time PCR, immunoprecipitation, mass spectrometry, immunofluorescence, and metabolite detection.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>We confirmed that Ig\u03ba, especially V\u03ba4-1\/J\u03ba3-Ig\u03ba, is highly expressed in human HCC cells. Ig\u03ba depletion inhibited HCC cell proliferation and migration in vitro, and hepatocyte-specific Ig\u03ba deficiency ameliorated HCC progression in mice with DEN and CCL4-induced HCC in vivo. Mechanistically, V\u03ba4-1\/J\u03ba3-Ig\u03ba interacts with electron transfer flavoprotein subunit \u03b1 (ETFA), delaying its protein degradation. Loss of Ig\u03ba led to a decrease in the expression of mitochondrial respiratory chain complexes III and IV, resulting in aberrant fatty acid \u03b2-oxidation (FAO) and lipid accumulation, which in turn inhibited HCC cell proliferation and migration.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings indicate that the Ig\u03ba\/ETFA axis deregulates fatty acid \u03b2-oxidation, contributing to HCC progression, which suggests that targeting fatty acid metabolism may be an effective HCC treatment strategy. The results of this study suggest that hepatocyte-derived V\u03ba4-1\/J\u03ba3-Ig\u03ba may serve as a promising therapeutic target for HCC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s13046-024-03203-8","type":"journal-article","created":{"date-parts":[[2024,10,8]],"date-time":"2024-10-08T23:32:11Z","timestamp":1728430331000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Hepatocyte-derived Ig\u03ba promotes HCC progression by stabilizing electron transfer flavoprotein subunit \u03b1 to facilitate fatty acid \u03b2-oxidation"],"prefix":"10.1186","volume":"43","author":[{"given":"Jingjing","family":"Guo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huining","family":"Gu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sha","family":"Yin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiongming","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qianqian","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weiyan","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yifan","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shenghua","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaofeng","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xunde","family":"Xian","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyan","family":"Qiu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,10,9]]},"reference":[{"issue":"6","key":"3203_CR1","doi-asserted-by":"publisher","first-page":"985","DOI":"10.1007\/s00018-009-0231-z","volume":"67","author":"S Zhang","year":"2010","unstructured":"Zhang S, Mao Y, Huang J, Ma T, Zhang L, Zhu X, et al. 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