Neddylation-dependent LSD1 destabilization inhibits the stemness and chemoresistance of gastric cancer

Int J Biol Macromol. 2024 Jan;254(Pt 3):126801. doi: 10.1016/j.ijbiomac.2023.126801. Epub 2023 Sep 7.

Abstract

Histone lysine-specific demethylase 1 (LSD1) expression has been evaluated in multiple tumors, including gastric cancer (GC). However, the mechanisms underlying LSD1 dysregulation in GC remain largely unclear. In this study, neural precursor cell-expressed developmentally down-regulated protein 8 (NEDD8) was identified to be conjugated to LSD1 at K63 by ubiquitin-conjugating enzyme E2 M (UBE2M), and this neddylated LSD1 could promote LSD1 ubiquitination and degradation, leading to a decrease of GC cell stemness and chemoresistance. Herein, our findings revealed a novel mechanism of LSD1 neddylation and its contribution to decreasing GC cell stemness and chemoresistance. Taken together, our findings may whistle about the future application of neddylation inhibitors.

Keywords: Gastric cancer; LSD1; Neddylation; Stemness; UBE2M.

MeSH terms

  • Drug Resistance, Neoplasm
  • Histone Demethylases
  • Humans
  • Stomach Neoplasms* / drug therapy
  • Ubiquitin-Conjugating Enzymes / genetics
  • Ubiquitin-Conjugating Enzymes / metabolism
  • Ubiquitination

Substances

  • Ubiquitin-Conjugating Enzymes
  • Histone Demethylases
  • UBE2M protein, human