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Repression of the PRELP gene is relieved by histone deacetylase inhibitors through acetylation of histone H2B lysine 5 in bladder cancer.

Published version
Peer-reviewed

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Authors

Shozu, Kanto 
Kaneko, Syuzo 
Shinkai, Norio 
Dozen, Ai 
Kosuge, Hirofumi 

Abstract

BACKGROUND: Proline/arginine-rich end leucine-rich repeat protein (PRELP) is a member of the small leucine-rich proteoglycan family of extracellular matrix proteins, which is markedly suppressed in the majority of early-stage epithelial cancers and plays a role in regulating the epithelial-mesenchymal transition by altering cell-cell adhesion. Although PRELP is an important factor in the development and progression of bladder cancer, the mechanism of PRELP gene repression remains unclear. RESULTS: Here, we show that repression of PRELP mRNA expression in bladder cancer cells is alleviated by HDAC inhibitors (HDACi) through histone acetylation. Using ChIP-qPCR analysis, we found that acetylation of lysine residue 5 of histone H2B in the PRELP gene promoter region is a marker for the de-repression of PRELP expression. CONCLUSIONS: These results suggest a mechanism through which HDACi may partially regulate the function of PRELP to suppress the development and progression of bladder cancer. Some HDACi are already in clinical use, and the findings of this study provide a mechanistic basis for further investigation of HDACi-based therapeutic strategies.

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Keywords

Research, Epigenetic Biomarkers, Gene expression, Extracellular matrix proteins, PRELP, HDACi, H2BK5ac, Bladder cancer

Journal Title

Clin Epigenetics

Conference Name

Journal ISSN

1868-7075
1868-7083

Volume Title

Publisher

Springer Science and Business Media LLC