Abstract
Abstract SET is a protein phosphatase 2A (PP2A) inhibitor and functions as an oncogene in multiple human cancer types. Here we revealed a novel phosphorylation site of SET in mitosis and its biological significance in tumorigenesis. We found that the mitotic kinase cyclin-dependent kinase 1 (CDK1) phosphorylates SET in vitroand in vivo at serine 7 during antimitotic drug-induced G2/M phase arrest and in normal mitosis. SET deletion resulted in massive mitotic defects including centrosome amplification, multipolar spindles, and chromosome missregregation. Moreover, we revealed that SET mitotic phosphorylation is required for proper mitotic progression and its oncogenic function in vitro and in xenograft animal models. Furthermore, we found STAT3 and p53 signaling are regulated by SET. Collectively, our findings suggest a novel layer of regulation for SET in mitosis and its role in tumorigenesis. (This is supported by Fred and Pamela Buffett Cancer Center Support Grant P30 CA036727) Citation Format: Ling Yin, Yongji Zeng, Jixin Dong. Cyclin-dependent kinase 1(CDK1)-mediated phosphorylation of SET in mitosis inhibits its oncogenic activity [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2543.
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