Telomerase is an enzyme that lengthens telomeres, the protective caps at the ends of chromosomes. Every time a cell divides, its telomeres get slightly shorter. When telomeres become too short, the cell often enters a state of senescence (a type of permanent cell cycle arrest) or undergoes apoptosis (programmed cell death).

Most normal somatic (non-reproductive) cells in adults do not produce telomerase and therefore experience telomere shortening with each cell division, which limits their replicative lifespan. This is often referred to as “replicative senescence.”

However, certain cells, such as stem cells and germ cells, do produce telomerase, which allows them to divide indefinitely without undergoing senescence or apoptosis. This is also true for most cancer cells, which often reactivate the expression of telomerase, allowing them to bypass replicative senescence and achieve “immortality.”

Telomerase reactivation in cancer is generally driven by mutations or alterations in the regulation of the genes encoding the components of the telomerase complex, most commonly the TERT gene, which encodes the catalytic subunit of telomerase. Telomerase reactivation allows cancer cells to maintain their telomere length despite frequent cell divisions, promoting their uncontrolled growth and survival.

On the other hand, reactivation of telomerase in normal cells is being explored as a potential strategy for treating diseases of aging and improving healthspan. However, this approach must be carefully controlled to avoid promoting the development of cancer. Researchers are actively studying the mechanisms of telomerase regulation and how to manipulate them for therapeutic purposes.