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A USP28-BRD4 axis contributes to the acceleration of breast cancer growth by hyperglycemia.
Cell Reports · · Journal Article
Li, Zhu + more
Abstract ↗AI summary
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Hyperglycemia stabilizes BRD4 and accelerates breast cancer growth, with the USP28-BRD4 axis requiring USP28 acetylation at lysine 702 (K702) for enhanced BRD4 stability.
- Why it matters: Diabetes worsens breast cancer progression, but how hyperglycemia promotes tumor growth through BRD4 regulation was unknown.
- What they did: Using proximity labeling proteomics, the study identified USP28 as a direct interactor and stabilizer of BRD4; USP28 deubiquitination and the USP28-BRD4 interaction required USP28 K702 acetylation controlled by KAT8 and SIRT1.
- The result: Under diabetes, reduced intracellular NAD+ impairs SIRT1, increases USP28-K702 acetylation, strengthens USP28-BRD4 binding, raises BRD4 stability, and makes the USP28-BRD4 axis required for hyperglycemia-driven breast cancer growth.
The findingWhy it mattersWhat they didThe result
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