BRAF mutation and NIS histone deacetylation

The BRAF V600E mutation impairs sodium iodide symporter (NIS) expression and thyroid cancer radioiodine refractoriness, but the underlying mechanism remains undefined. In this study, Zhang and colleagues hypothesized that histone deacetylation at the NIS (SLC5A5) promoter is the mechanism. Using the chromatin immunoprecipitation approach, they examined histone acetylation status of the lysine residues. Their results uncover an epigenetic mechanism for BRAF V600E-promoted NIS silencing involving histone deacetylation at critical regulatory regions of the NIS promoter and provide further support for combination therapy which targets major signaling pathways and histone deacetylase to restore thyroid gene expression in thyroid cancer.

Read the full article at Zhang et al. (2014) Endocrine-Related Cancer 21 161–173; DOI: 10.1530/ERC-13-0399