Loss of Setd2 promote Kras-induced acinar-to-ductal metaplasia and epitheliamesenchymal transition during pancreatic carcinogenesis

TCGA(PAAD) public database and PDAC tissue array with SETD2/H3K36me3 staining was used to investigate the clinical relevance of SETD2 in PDAC. Furthermore, to define the role of SETD2 in the carcinogenesis of PDAC, we crossed conditional Setd2 knockout mice (PdxcreSetd2flox/flox) together with with KrasG12D mice. Moreover, to examine the role of SETD2 after ductal metaplasia, Crisp/cas9 was used to deplete Setd2 in PDAC cells. RNA-seq and H3K36me3 Chip-seq were performed to uncover the mechanism. Overall design: RNA-seq and H3K36me3 Chip-seq were performed in mouse acinar cell and KPC1199 cell line.