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Regulation of hTERT transcription: a target of cellular and viral mechanisms for immortalization and carcinogenesis

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Abstract

A hallmark of human cancer cells is immortal cell growth, which is associated with telomere maintenance by telomerase. The transcriptional regulation of the human telomerase reverse transcriptase (hTERT) gene is a major mechanism that negatively and positively controls telomerase activity in normal and cancer cells, respectively. A growing body of data suggests that various cellular and viral factors and pathways involved in cell senescence, immortalization and carcinogenesis act on the hTERT promoter. The activity of the hTERT promoter is regulated, either directly or through signaling pathways, by oncogene products (e.g., Myc and Ets families) and tumor suppressor proteins (e.g., BRCA1). Endogenous factors involved in the physiological repression of the hTERT gene have also been revealed by chromosome transfer experiments. The integration of viral genomes in the hTERT locus can lead to hTERT activation and telomerase induction. Here, we summarize these findings and pay special attention to recent findings with relevance to the endogenous regulatory mechanisms of hTERT transcription.

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Abbreviations

ChIP:

chromatin immunoprecipitation

HBV:

hepatitis B virus

HIF:

hypoxia-inducible factor

HPV:

human papillomavirus

hTERT:

human telomerase reverse transcriptase

MMCT:

microcell-mediated chromosome transfer

RNAi:

RNA interference

siRNA:

small interfering RNA

TRRAP:

transformation-transactivation domain-associated protein.

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  1. Laboratory of Biosystems and Cancer, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Building 37, Room 5046, Bethesda, MD, 20892, USA

    Izumi Horikawa, Eriko Michishita & J. Carl Barrett

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  1. Izumi Horikawa
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  2. Eriko Michishita
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Correspondence to Izumi Horikawa.

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Horikawa, I., Michishita, E. & Barrett, J. Regulation of hTERT transcription: a target of cellular and viral mechanisms for immortalization and carcinogenesis. Cytotechnology 45, 23–32 (2004). https://doi.org/10.1007/s10616-004-5122-4

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