Mitotic centromere-associated kinase (MCAK/Kif2C) regulates cellular senescence in human primary cells through a p53-dependent pathway

AbstractMitotic centromere-associated kinase (MCAK/Kif2C) plays a critical role in chromosome movement and segregation with ATP-dependent microtubule depolymerase activity. However, its role in cellular senescence remains unclear. MCAK/Kif2C expression decreased in human primary cells under replicative and premature senescence. MCAK/Kif2C down-regulation in young cells induced premature senescence. MCAK/Kif2C overexpression in old cells partially reversed cell senescence. Senescence phenotypes by MCAK/Kif2C knockdown were observed in p16-knockdown cells, but not in p53-knockdown cells. These results suggest that MCAK/Kif2C plays an important role in the regulation of cellular senescence through a p53-dependent pathway and might contribute to tissue/organism aging and protection of cellular transformation