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Telomerase: Structure and Function

  1. Jerry W Shay

Published Online: 18 OCT 2013

DOI: 10.1002/9780470015902.a0006167.pub2



How to Cite

Shay, J. W. 2013. Telomerase: Structure and Function. eLS. .

Author Information

  1. University of Texas Southwestern Medical Center, Dallas, Texas, USA

  1. Based in part on the previous version of this eLS article ‘Telomerase: Structure and Function’ (2005) by Nathaniel J Hansen, Joseph C Poole, Lucy G Andrews and Trygve O Tollefsbol.

Publication History

  1. Published Online: 18 OCT 2013


In contrast to normal cells, tumour cells generally have short telomere lengths and show no continuing loss of telomere length with successive cell divisions, suggesting that telomere stability may be required for cells to escape from replicative senescence and proliferate indefinitely. Most, but not necessarily all, malignant tumours are immortal to sustain their growth, thus, the cellular ribonucleoprotein (reverse transcriptase) enzyme complex termed telomerase may be a rate-limiting step required for the continuing proliferation of advanced cancers. Telomerase, the enzyme that completes deoxyribonucleic acid (DNA) replication at the termini of eukaryotic chromosomes, is an important factor in DNA replication, chromosomal stability and tumorigenesis.

In human tumours, telomere length is maintained by a balance between processes that lengthen telomeres (telomerase) and processes that shorten telomeres (lack of complete lagging DNA strand synthesis ‘end replication problem’ and other end processing events). Telomerase stabilises telomere length by adding TTAGGG repeats onto the telomeric ends of the chromosomes, thus compensating for the continued erosion of telomeres that occurs in its absence. As telomerase is expressed in almost all human cancers, approaches for inhibiting telomerase as a target for cancer therapeutics are currently progressing through clinical trials.

Key Concepts:

  • Telomeres, the ends of human chromosomes progressively shorten throughout life in all dividing human cells and when critically shortened become ‘uncapped’ leading to a DNA damage signal and then undergo growth arrest termed replicative senescence (cell ageing).

  • A hallmark of cancer cells is unlimited cell growth.

  • Advanced cancer cells accomplish immortality almost universally by activating or upregulating the ribonucleoprotein complex termed telomerase.

  • Telomerase is composed of two essential components, TERT (reverse transcriptase component) and TERC (functional or template RNA that recognises the ends of chromosomes).

  • Telomerase is expressed during early human development and remains silent in almost all human tissues except transiently amplified stem cells throughout life.

  • Approximately 90% of all human cancers express telomerase activity.

  • A small fraction of human tumours do not express telomerase and some of these may engage a DNA recombination mechanism to maintain telomeres termed ALT, alternative lengthening of telomeres.

  • Introduction of hTERT into normal telomerase silent cells is sufficient to immortalise cells in appropriate culture conditions without the cells becoming cancerous.

  • As telomerase is almost a universal oncology target, inhibiting telomerase should be a potent anticancer therapeutic target.


  • telomerase;
  • telomeres;
  • senescence;
  • ageing;
  • immortal;
  • cancer