BRD4 ChIP-seq in JQ1 treatment and control in MDA-MB-231 cells.

Aberrant expression of m6A writer complex has been reported across human cancers, resulting in abnormal m6A epitranscriptome that drives tumorigenesis. But the regulatory mechanism remains unknown. Here, we identified an unappreciated interplay between the histone acetyl-lysine reader BRD4 and the m6A methyltransferase complex (MTC) across human cancers. BRD4 directly stimulates transcript expression of seven MTC subunits, allowing the maintenance of nuclear METTL3/METTL14 abundance and the formation of functional writer complex to catalyze m6A modification. Overall design: ChIP-seq performed in this study was designed to uncover the role of BRD4-mediated regulation of gene transcription.