ATAD2B governs epigenetic silencing of the epithelial program to fuel cancer metastasis and neuronal migration.

ATAD2B is an H3K27ac reader that is essential for cell migration, enforcing a mesenchymal state in EMT onset and supporting lung metastasis and neuronal migration.

• Why it matters: EMT-linked changes in H3K27ac are known, but the chromatin readers that decode these signals to control motility in cancer and brain development are unclear.
• What they did: Multi-omics profiling at EMT onset showed ATAD2B targets H3K27ac at active epithelial identity genes, uses its bromodomain to recruit HDAC1, and silences them.
• The result: ATAD2B loss reduces migration and invasion in breast cancer lines and patient-derived organoids, while overexpression accelerates in vivo lung metastasis and is linked to poor patient survival, and it promotes newborn neuron migration.

AI summary of the abstract · may contain errors · not medical advice · read the paper.