ATAD2B silences the epithelial program to fuel cancer metastasis and neuronal migration

ABSTRACT: Epithelial-to-mesenchymal transition (EMT) is a pivotal developmental program that is frequently co-opted to drive cancer aggressiveness and metastasis. While the dynamic remodelling of histone H3 lysine 27 acetylation (H3K27ac) landscapes is a hallmark of EMT, the specific chromatin readers decoding these epigenetic signals remain largely unknown. Here, we identify ATAD2B as a novel H3K27ac reader essential for cell migration in both cancer metastasis and brain development. Multi-omics profiling revealed that, at EMT onset, ATAD2B targets H3K27ac at active epithelial identity genes via its bromodomain and recruits HDAC1 to epigenetically silence them, enforcing a mesenchymal state. ATAD2B loss impairs migration and invasion in breast cancer lines and Patient-Derived organoids, whereas its

SUBMITTER: Arun Mahesh 

PROVIDER: S-SCDT-10_1038-S44318-026-00933-7 | biostudies-other |

REPOSITORIES: biostudies-other