Telomere End Protection in Stem Cells and Cancer Cells

Loss of telomere DNA in normal somatic cells is a major alteration upon ageing. Stem cells and progenitor cells also lose telomere DNA, but at a slower rate than normal cells due to activation of a low level of telomerase activity. Embryonic stem cells exhibit strong telomerase activity, maintain telomere length, and are resistant to DNA damage. In contrast, hematopoietic stem cells, which have weak telomerase activity, are sensitive to DNA damage. The shelterin complex is involved in t-loop formation, a mechanism thought to protect chromosome ends from DNA damage that induces telomere dysfunction. Telomere dysfunction in stem cells brought on by ageing as well as DNA damage has been shown to partake in various age-related diseases. This review illustrates the importance of the telomere end protection mechanism in normal, stem cells and cancer stem cells.