The abstract is read at the publisher; the summary is JClub's.
Restoring RARγ in enzalutamide-resistant 22Rv1 prostate cancer cells recruits a RARγ complex with TACC1 and SMARCA5, reshaping the AR cistrome toward active luminal programs.
- Why it matters: Epigenomic control of AR signaling is linked to resistance to enzalutamide, but how RARγ influences AR chromatin targeting and lineage plasticity is unclear.
- What they did: The study restored RARγ in enza-resistant 22Rv1 and LNCaP C4-2 cells, mapping AR cistrome and H3K27ac overlap, assessing SMARCA5 promoter-proximal binding, and testing a miR-96 antagomir that targets RARγ.
- The result: RARγ restoration expanded and redistributed AR binding to active promoters, enhancers, and super-enhancers, increased luminal differentiation programs, and antagonized ONECUT2-linked alternative-lineage signatures associated with lineage plasticity and enza responsiveness in murine models and human cohorts.
The findingWhy it mattersWhat they didThe result
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