SUMOylation involves in β-arrestin-2-dependent metabolic regulation in breast cancer cell

• Published in: Biochemical and biophysical research communications Vol. 529; no. 4; pp. 950 - 956
• Main Authors: Dong, Changsheng, Li, Ying, Niu, Qun, Fang, Houshun, Bai, Jie, Yan, Yinjie, Gu, Chuan, Xiao, Ning
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 03.09.2020
• Subjects: beta-Arrestin 2 - genetics; beta-Arrestin 2 - metabolism; Breast cancer cell; Cell Line, Tumor; Cell Movement; Cell Proliferation; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Gene Ontology; HEK293 Cells; Humans; Intracellular Signaling Peptides and Proteins - genetics; Intracellular Signaling Peptides and Proteins - metabolism; MCF-7 Cells; Metabolic Networks and Pathways - genetics; Metabolic regulation; Molecular Sequence Annotation; Protein Processing, Post-Translational; Receptors, Interleukin-1 Type I - genetics; Receptors, Interleukin-1 Type I - metabolism; Signal Transduction; SUMOylation; β-Arrestin-2; CRISPR; SUMO; TRAF6; Metabolic regulation; Breast cancer cell; SUMOylation; Cas9; IL-1R; β-Arrestin-2
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2020.06.033

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. 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. [Display omitted]