ArticleNature communications2026
The UFL1-AKT positive feedback loop promotes breast cancer progression by enhancing lipid synthesis.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Narrative review-the emerging role, functions, and mechanisms of UFMylation in cancers.Translational cancer research · 2026Review
- The Role of Lipid Metabolism in the Progression of Breast Cancer.Journal of Cancer · 2026Review
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Authors and funding
18 authors.
Funding
Abstract
UFMylation, a ubiquitin-like modification, is crucial for cellular processes and is linked to human diseases, including cancer. However, its role in cancer remains unclear. Here, we report that UFL1 promotes breast tumor growth by remodeling lipid metabolism. Mechanistically, UFL1 interacts with and UFMylates AKT, enhancing its localization at the endoplasmic reticulum and phosphorylation by PDK1 and mTORC2, thereby increasing AKT-mediated lipid synthesis. Moreover, AKT phosphorylates UFL1, boosting its activity. Thus, UFL1 and AKT form a positive feedback loop, accelerating lipid synthesis and breast tumor growth. Clinically, UFL1 levels are increased in human breast tumors and are associated with poor clinical outcomes in breast cancer patients. Importantly, UFMylation inhibitors sensitize breast cancer cells to AKT inhibitors and anticancer drugs. Our findings reveal a critical role for UFMylation in lipid metabolism and identify the UFL1-AKT axis as a potential therapeutic target in breast cancer.
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