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Roganowicz, M.

Publications and source records attributed to Roganowicz, M..

2 recordsLinked to original sources

BAZ2A-RNA mediated association with TOP2A and KDM1A represses gene expression in prostate cancer

BAZ2A is the repressor of rRNA genes that are transcribed by RNA Polymerase I. In prostate cancer (PCa), however, BAZ2A function goes beyond this role since it can also repress other genes that are frequently silenced in metastatic disease. However, the mechanisms of BAZ2A-mediated repression in PCa remain elusive. Here we show that BAZ2A represses genes implicated in PCa through its RNA-binding TAM domain using mechanisms differing from rRNA gene silencing. While TAM domain mediates BAZ2A recruitment to rRNA genes, in PCa cells this is not required for BAZ2A association with target genes. Instead, BAZ2A-TAM domain in association with RNA mediates the interaction with topoisomerase 2A (TOP2A) and histone demethylase KDM1A, whose expression positively correlates with BAZ2A levels in both localized and aggressive PCa. Pharmacological inhibition of TOP2A and KDM1A activities upregulates the expression of BAZ2A-repressed genes that are regulated by a class of inactive enhancers bound by BAZ2A whereas rRNA genes are not affected. Our findings showed a novel RNA-based mechanism of gene regulation in PCa. Further, the data indicate that RNA-mediated interactions between BAZ2A and TOP2A and KDM1A repress genes critical to PCa and may prove to be useful to stratify prostate cancer risk and treatment in patients.

molecular biology↗

BAZ2A association with H3K14ac is required for the dedifferentiation of prostate cancer cells into a cancer stem-like state

Prostate cancer (PCa) is one of the most prevalent cancers in men. Cancer stem cells are thought to be associated with PCa relapse. Here we show that BAZ2A is required for the transition of PCa cells into a cancer stem-like state. BAZ2A genomic occupancy in PCa cells coincides with H3K14ac enriched chromatin regions. This association is mediated by BAZ2A-bromodomain (BAZ2A-BRD) that specifically binds H3K14ac. BAZ2A associates with inactive enhancers marked by H3K14ac and repressing transcription of genes frequently silenced in aggressive and poorly differentiated PCa. BAZ2A-mediated repression is also linked to EP300 that acetylates H3K14ac. BAZ2A-BRD mutations or treatment with inhibitors abrogating BAZ2A-BRD/H3K14ac interaction impair the transition of PCa cells into a stem-like state. Furthermore, pharmacological inactivation of BAZ2A-BRD impairs Pten-loss oncogenic transformation of prostate organoids. Our findings indicate a role of BAZ2A-BRD in PCa stem cell features and suggest potential epigenetic-reader therapeutic strategies to target BAZ2A in aggressive PCa.

molecular biology↗