SPOP suppresses prostate cancer through regulation of CYCLIN E1 stability

• Published in: Cell death and differentiation Vol. 26; no. 6; pp. 1156 - 1168
• Main Authors: Ju, Lin-Gao, Zhu, Yuan, Long, Qiao-Yun, Li, Xue-Jing, Lin, Xiang, Tang, Shan-Bo, Yin, Lei, Xiao, Yu, Wang, Xing-Huan, Li, Lianyun, Zhang, Lei, Wu, Min
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.06.2019; Nature Publishing Group
• Subjects: 13/106; 13/109; 13/31; 13/89; 38/39; 631/45/612/1244; 631/67/1244; 64; 64/60; 96; 96/35; Apoptosis; Biochemistry; Biomedical and Life Sciences; Cell Biology; Cell Cycle Analysis; Cell Line; Cell Movement; Cell Proliferation; Cyclin E - genetics; Cyclin E - metabolism; Cyclin-dependent kinase 2; Humans; Life Sciences; Male; Nuclear Proteins - metabolism; Oncogene Proteins - genetics; Oncogene Proteins - metabolism; Prostate cancer; Prostatic Neoplasms - metabolism; Prostatic Neoplasms - pathology; Protein Stability; Repressor Proteins - metabolism; Signal Transduction; Stem Cells; Substrate specificity; Tumor cell lines; Tumorigenesis; Ubiquitination

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 for SPOP. SPOP directly interacts with CYCLIN E1 and specific regulates its stabili...