The role of sentrin-specific protease 2 substrate recognition in TGF-β-induced tumorigenesis.

ABSTRACT: Smad4, a common-mediator of Smads, plays a central role in forming complexes with receptor-phosphorylated Smads, and then transduces transforming growth factor (TGF)-β signals into the nuclei. Although many cellular factors are involved in TGF-β induced epithelial-to-mesenchymal transition (EMT) and cell migration, very little is known with the mechanism of Smad4 regulation on pro-oncogenes response by TGF-β. Herein, we demonstrate the interaction of Sentrin-specific protease 2 (SENP2) with Smad4 through SENP2 residue 363~400. The same segment is also important for desumoylation of Smad4, and able to relieve sumoylation-mediated TGF-β repression. The SENP2^363~400 segment is critical for TGF-β-induced cell migration, which is correlated with SENP2^363~400 deletion mutan

SUBMITTER: Chang CC 

PROVIDER: S-EPMC6023881 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature