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Telomerase activity is detected in most malignant human tumors, but not found in normal somatic cells except for a few cell lines. Telomere is located on the end of eukaryotic chromosomes and must be of sufficient length to ensure chromosome stabilization. It is hypothesized that the reactivated enzyme, telomerase, in malignant tumors maintains the telomere length towards attrition during cell replication. In contrast, normal somatic cells are terminated by one of thep53 functions caused by signals promoting a critically shortened telomere region. In this study, wild typep53 gene was introduced into a head and neck squamous cell carcinoma (HNSCC-2p) cell line by a lipofectin method. We examined whether wild typep53 plays a role in regulating telomerase activity, human telomerase reverse transcriptase (hTERT) protein production, and hTERT mRNA expression. The cells, which were derived from a tongue squamous cell carcinoma, had two point mutations ofp53 and telomerase activity. Telomerase activity, hTERT mRNA expression, and hTERT production as protein were examined by telomerase repeat amplification protocol (TRAP), reverse transcriptase (RT)-PCR, and Western blotting, respectively. Telomerase activity, hTERT mRNA expression, and hTERT showed a down-regulation 24 and 48 hours after wild type p53 introduction. These data suggest that wild typep53 down-regulates telomerase activity and hTERT production as protein by repressing hTERT transcription.

Study on down-regulation of telomerase activity in oral squamous cell carcinoma cells transfected with wild-type p53 gene