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

Biochem Biophys Res Commun. 2020 Sep 3;529(4):950-956. doi: 10.1016/j.bbrc.2020.06.033. Epub 2020 Jul 30.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 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*
  • Molecular Sequence Annotation
  • Protein Processing, Post-Translational*
  • Receptors, Interleukin-1 Type I / genetics
  • Receptors, Interleukin-1 Type I / metabolism
  • Signal Transduction
  • Sumoylation
  • beta-Arrestin 2 / genetics*
  • beta-Arrestin 2 / metabolism

Substances

  • ARRB2 protein, human
  • IL1R1 protein, human
  • Intracellular Signaling Peptides and Proteins
  • Receptors, Interleukin-1 Type I
  • Tifab protein, human
  • beta-Arrestin 2