作者: Hanyu Rao , Xiaoxue Li , Min Liu , Jing Liu , Wenxin Feng
DOI: 10.1101/2020.07.13.200220
关键词:
摘要: Clear cell renal carcinoma (ccRCC) is a largely incurable disease that highly relevant to epigenetic regulation including histone modification and DNA methylation. SET domain-containing 2 (SETD2) predominant methyltransferase catalyzing the trimethylation of H3 Lysine 36 (H3K36me3) its mutations are clear (ccRCC). However, physiology role in ccRCC remains unexplored. Here we report Setd2 deletion impairs {beta}-catenin destruction complex facilitate formation c-MYC-generated polycystic kidney (PKD) model, which can be relieved by an inhibitor {beta}-catenin-responsive transcription. Clinically, SETD2 loss widely observed samples, negatively correlated with expression some members complex, but positively activation Wnt/{beta}-catenin signaling. Our findings thus highlight previously unrecognized SETD2-mediated H3K36me3 pathway ccRCC. SummaryOur for first time reveal shed light on molecular mechanisms underlying disorders.