BAZ2A, also known as bromodomain adjacent to zinc finger domain protein 2A, is an epigenetic regulator. It affects the transcription of ribosomal RNA and is involved in chromatin remodeling, which is crucial for regulating gene expression, maintaining genome architecture, and influencing various biological processes [3,2].

In prostate cancer, BAZ2A is required for cells with a cancer-stem-like state. Its genomic occupancy coincides with H3K14ac-enriched chromatin regions. BAZ2A associates with inactive enhancers marked by H3K14ac, repressing transcription of genes often silenced in aggressive and poorly differentiated prostate cancer. Inhibiting BAZ2A-bromodomain (BAZ2A-BRD) impairs prostate cancer stem cells and Pten-loss oncogenic transformation of prostate organoids [1].

In ground-state pluripotent stem cells, BAZ2A safeguards genome architecture. It interacts with SNF2H, TOP2A, and cohesin on ESC chromatin. Depletion of BAZ2A increases chromatin accessibility at B compartments and affects H3K27me3 genome occupancy in a TOP2A-dependent manner [2].

In mammalian liver regeneration, in vivo CRISPR screening identified Baz2a as a regulator. Inhibiting BAZ2a with specific bromodomain inhibitors accelerates liver healing after various injuries and also shows improved healing in an inflammatory bowel disease model [4].

In summary, BAZ2A plays essential roles in maintaining genome architecture, regulating gene expression in stem cells, and promoting cancer stem-like states in prostate cancer. In vivo studies, including gene-knockout-like strategies in mouse models, have revealed its significance in these biological processes and potential as a therapeutic target in diseases such as prostate cancer and for enhancing tissue repair in liver and other tissues [1,2,4].