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Fragmentation and rapid shortening of telomere in HeLa cells in the early phase of hydroxyl radical-induced apoptosis

In order to maintain genomic stability, cells recognize and response to DNA damage by either cell cycle arrest or apoptosis. Telomeres are the special DNA sequences at chromosome termini that plays important role in maintaining chromosomal stability. Telomeric DNA has been shown to be much more susceptible to damage than non-telomere sequences. Recent studies suggest that telomere disruption can trigger apoptosis in certain cell types, mimicking a major cellular response to DNA damage. In this work, we studied the DNA damage at the telomere region during hydroxyl radical-induced apoptosis in HeLa cells. It was found that HeLa cells experienced telomere strand fragmentation and rapid telomere shortening following treatment of H2O2 well before caspase-3 activation and apoptosis. The percentage of cells undergoing apoptosis correlated with the extent of telomere strand fragmentation. Introducing telomere oligonucleotide into cells induced cell cycle arrest in S-phase and apoptosis. We speculate that telomere fragments released from chromosomes might serve as triggering signal in DNA damage-induced apoptosis in the HeLa cells.