SPOP suppresses prostate cancer through regulation of CYCLIN E1 stability

• DOI: 10.1038/s41418-018-0198-0
• Publication Date: 2018-09-20T08:46:14Z
• Authors: Lin-Gao Ju; Yuan Zhu; Qiao-Yun Long; Xue-Jing Li; Xiang Lin; Shan-Bo Tang; Lei Yin; Yu Xiao; Xing-Huan Wang; Lianyun Li; Lei Zhang; Min Wu
• Keywords: Cyclin A; Cyclin E1; Cyclin D; Cyclin E; Cyclin A2

SPOP is one of the important subunits for CUL3/SPOP/RBX1 complex tightly connected with tumorigenesis. However, its exact roles in different cancers remain debatable. Here, we identify CYCLIN E1, as a novel substrate SPOP. directly interacts E1 and specific regulates stability prostate cancer cell lines. SPOP/CUL3/RBX1 through poly-ubiquitination. CDK2 competes interaction, suggesting that probably CDK2-free E1. expression rescued proliferation, migration, tumor formation suppressed by Furthermore, found selectively substrates' signaling pathways CCRC lines, complicated mechanisms exist to regulate specificity. Altogether, have revealed mechanism suppressing provided evidence show has dual functions CCRC.