ArticleCell death and differentiation2026
JAB1/CRL4B complex represses PPARG/ACSL5 expression to promote breast tumorigenesis.
Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Adipocyte-rich microenvironment promotes TNBC progression through SIRT6-associated ACSL5 dysregulation and lipid storage-associated phenotypes.Journal of experimental & clinical cancer research : CR · 2026Article
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Authors and funding
17 authors.
Funding
Abstract
Fatty acid metabolism is critical for tumor progression, supplying bioenergetic and biosynthetic substrates to rapidly proliferating cancer cells. However, the precise mechanisms by which fatty acid metabolism influences breast cancer progression remain unclear. In this study, we aimed to explore the molecular mechanism by which C-Jun activation domain-binding protein-1 (JAB1) promotes breast cancer progression through regulating fatty acid metabolism. The JAB1 is identified as an oncogene in breast cancer. JAB1 promotes cell proliferation, invasion, and stemness by stabilizing CUL4B protein. Mechanistically, JAB1 forms a transcriptional repressor complex with the Cullin 4B-Ring E3 ligase (CRL4B) complex, co-occupying the promoters of key fatty acid metabolism genes, PPARG and ACSL5, thus leading to their transcriptional repression. This activates fatty acid metabolism, increasing mitochondrial oxygen consumption and supporting the energetic demands of tumor cells. Notably, JAB1 inhibition reverses chemotherapy resistance associated with CUL4B overexpression. These findings underscore the pivotal role of JAB1 in regulating breast cancer progression and indicate that JAB1 inhibitors could serve as promising therapeutics for patients with elevated CUL4B expression.
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