β-arrestin-2, a multifunctional adaptor protein, was originally identified as a negative regulator of G protein-mediated signaling. We previously revealed that SUMOylation as a novel mechanism modulates β-arrestin-2-mediated IL-1R/TRAF6 signaling. However, the potential role of β-arrestin-2 SUMOylation in tumor cells was incompletely explored. In this study, we showed that SUMOylation deficiency of β-arrestin-2 resulted in slower migration of breast cancer cells, but little effect on the cell proliferation. Importantly, our data indicated that SUMOylation involves in β-arrestin-2-dependent metabolic regulation, suggesting a potent regulatory pattern for β-arrestin-2-mediated biological functions of tumor cells.
Keywords: Breast cancer cell; Metabolic regulation; SUMOylation; β-Arrestin-2.
Copyright © 2020 Elsevier Inc. All rights reserved.