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In a surprise twist, an enzyme that “immortalizes” cancer cells also prevents tumors and slows a key stage in normal cell death, according to new research from the University of Maryland and the National Institutes of Health.
The study published this week in the Proceedings of the National Academy of Sciences reveals a new role for telomerase. Its only previously known function in normal tissue was to protect certain cells that divide regularly, such as embryonic, sperm, adult stem and immune cells. Scientists thought telomerase was turned off in other cells, except in cancerous tumors, where it promotes unlimited cell division.
The new research found that telomerase reactivates in normal adult cells at a critical point in the aging process. Just before cell death, a burst of telomerase buffers cells from the stresses of aging, slowing the process and reducing DNA damage that could lead to cancer.
“Our work shows, for the first time, that there is a role for telomerase in adult cells beyond promoting tumor formation,” said Kan Cao, senior author and an associate professor of cell biology and molecular genetics.
Telomerase prevents the shortening of telomeres—a specialized DNA-protein structure at the end of a cell’s chromosomes that protect the chromosomes from damage. In normal adult cells, telomerase is turned off and telomeres shorten with every cell division until they reach a critical length, when cells stop dividing and either die or experience DNA damage that could cause malignancies.
Cao said the next step for researchers is to find out how telomerase expression is turned on as cells approach critical telomere length and to explore the underlying mechanisms by which telomerase acts as a buffer against the stresses of shortening telomeres.
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