Rapid cell senescence-associated changes in galactosylation of N-linked oligosaccharides in human lung adenocarcinoma A549 cells.

Abstract Rapid senescence was induced into human lung adenocarcinoma A549 cells by transforming growth factor-β1. Lectin blot analysis of membrane glycoprotein samples showed that the binding of Ricinus communis agglutinin-I to protein bands increased markedly while those of other lectins together with protein components did not change significantly with senescence. This indicates that the β-1,4-galactosylation of N-linked oligosaccharides is stimulated by rapid senescence. Analysis of the enzymatic background of senescence showed 1.5 times higher β-1,4-galactosyltransferase (β-1,4-GalT) activity and 2–5 times higher expression levels of β-1,4-GalT II, III, V, and VI genes are associated with rapid senescence. Incubation of the cells on RCA-I-coated plates in the absence of fetal calf serum showed that the viability of the senescent cells is half that of the control cells. Therefore, it is hypothesized that galactose residues expressed by rapid senescent can induce a lethal signal in cells if they interact with appropriate receptors.