Lysine-specific demethylase 1 (LSD1) suppresses cellular senescence by riboflavin uptake-dependent demethylation activity.

ABSTRACT: Cellular senescence is defined as a permanent proliferation arrest caused by various stresses, including DNA damage. We have recently identified the riboflavin transporter SLC52A1, whose expression is increased in response to senescence-inducing stimuli. Interestingly, increased expression of SLC52A1 suppresses cellular senescence through the uptake of riboflavin and an increase in intracellular flavin adenine dinucleotide (FAD), an enzyme cofactor synthesized from riboflavin. However, how FAD suppresses cellular senescence has not been fully elucidated. Therefore, in this study, we focused on lysine-specific demethylase 1 (LSD1), which uses FAD as a cofactor. First, we found that LSD1 inhibition promoted DNA damage-induced cellular senescence, whereas ectopic expression of LSD1 suppressed

SUBMITTER: Osumi T 

PROVIDER: S-EPMC11847913 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature