Down-regulation of Aurora B kinase induces cellular senescence in human fibroblasts and endothelial cells through a p53-dependent pathway

Aurora B kinase (Aurora-B) functions in chromosome segregation and cleavage of polar spindle microtubules. However, its role in cellular senescence remains elusive. Here, we investigated Aurora-B effects on cellular senescence in human fibroblasts and endothelial cells. Aurora-B levels were reduced during replicative senescence and premature senescence by adriamycin. Aurora-B overexpression in old cells partially reversed senescence phenotypes. In contrast, Aurora-B down-regulation accelerated cellular senescence. p53 knockdown but not p16 knockdown inhibited cellular senescence by Aurora-B reduction. These results suggest that Aurora-B might function in the regulation of cellular senescence of human primary cells via a p53-dependent pathway.

► Aurora-B levels decreased during replicative senescence and premature senescence. ► Aurora-B overexpression in old cells partially reversed senescence phenotypes. ► In contrast, Aurora-B down-regulation accelerated cellular senescence. ► p53 knockdown but not p16 knockdown inhibited cell senescence by Aurora-B down-regulation. ► Aurora-B may regulate cellular senescence of human primary cells via a p53 pathway.