Telomerase is an enzyme found inside our cells, which may be related to the aging process. It adds short, repetitive “caps” to our DNA strands. These caps are called “telomeres.”
Each time our cells divide, they must replicate their DNA so that each daughter cell gets a full set of operating instructions. However, with each cell division, a small part of the DNA strand’s protective telomeres are lost.
Scientists believe that the loss of telomeres leads to eventual loss of important, coding regions of DNA, and that this impairs cells’ ability to divide and produce healthy daughter cells over time.
This idea is supported by studies finding that mice which lack the enzyme telomerase appear to age and develop age-related diseases faster than normal mice. These effects of premature aging can actually be reversed by artificially adding telomerase to mouse cells!
These findings have led some scientists to speculate that telomerase may be a potential “fountain of youth” which, if used properly, could stop the aging process and keep our cells young and healthy indefinitely. Other scientists, however, caution that there is not sufficient data to believe that is true, and that artificially adding telomerase to our bodies could increase our risk of cancer.
The relationship of telomerase to cancer is not yet fully understood. On one hand, studies in humans have found that people with very short telomeres are much more likely to get cancer, perhaps because those cells are more likely to suffer DNA damage which can lead to cancer. This finding suggests that use of artificial telomerase may prevent cancer from occurring.
On the other hand, scientists point out that overactive telomerase is found in many cancer cells, and that its activity may actually be one factor that enables cancer cells to divide virtually without limit, overtaking healthy cells. If this is the case, “overdosing” on telomerase may feed cancer cells more than healthy cells, and lead to an increase in dangerous cancers.
There is not enough data yet to know how artificial telomerase would affect humans in the long-term. More research on this subject is needed.
Function of Telomerase
“Telomeres” are lengths of short, highly repetitive nucleotide sequences found on the ends of our DNA strands. Unlike the vital parts of our DNA, telomeres do not contain information needed to make proteins. Instead, they act as a buffer or “cap” to protect the vital coding regions.
Each time a cell divides, it must replicate its DNA. Some nucleotides are lost from the end of DNA strands in the process of replication. That means that as time goes on, the telomeres in your body’s cells get shorter. When the telomeres are entirely gone, potentially vital regions of DNA that code for proteins will begin to be lost.
The function of telomerase is to add more nucleotides to the telomeres, regenerating these protective “caps” and helping the vital regions of our DNA to avoid damage.
Studies have shown that artificially adding telomerase to mice whose cells don’t naturally produce it can reverse their premature symptoms of aging.
However, it’s not currently known how taking artificial telomerase would affect the health of human volunteers. One study found that taking substances which boost the activity of telomerase did lengthen telomeres in some people – only those whose telomeres were very, very short at the start of the trial.
In theory, this could mean that the telomerase was preventing the deaths or mutations of cells that would otherwise have died. But it was not clear what effect this had on patient’s health, and long-term cancer rates in these patients are not known.
Some scientists believe that telomerase has additional functions in the cell’s aging process, beyond just extending telomeres to protect our DNA. But as of right now, this is not certain. More research is needed.
Telomerase has a core that is similar to the enzyme “reverse transcriptase,” also sometimes called “RNA transcriptase.” Reverse transcriptase is an enzyme that makes strands of DNA based on RNA templates – hence the name, since it performs the reverse of normal DNA-to-RNA transcription.
This similarity makes sense, since telomerase does assemble new DNA sequences, just like reverse transcriptase. Some scientists believe that telomerase may have evolved from a form of reverse transcriptase into this specialized enzyme which replenishes DNA strands’ protective “caps” in the distant past.
In some species, only one subunit of the telomerase enzyme is needed to repair telomeres. However, human telomerase is only functional as a dimer – meaning that two identical telomerase units must join together in order to perform the enzyme’s function.
The term “dimer” comes from the root words “di” for “two” and “mer” for “parts.”
The image below shows a telomerase protein wrapped around a DNA strand.
Telomerase and Cancer
The relationship of telomerase to cancer is not yet fully understood. This seems to be one case where the ancient philosophers who counseled “all things in moderation” were correct.
On one hand, it is possible that having too little telomerase could increase the risk of cancer. One study found that people with very short telomeres were a whopping three times more likely to get cancer within a decade than people with long telomeres.
One possible mechanism for this is obvious: cells with little or no protective “caps” on the ends of their DNA strands are more likely to suffer damage to coding regions of DNA. Mutations to coding regions of DNA could cause cancer.
On the other hand, it is also known that most cancers have mutated, over-active versions of telomerase. It is thought that these over-active telomerase enzymes are actually keeping the cancer cells alive, allowing them to divide rapidly an unlimited number of times without aging or dying. This raises the troubling prospect that too much telomerase could help cancer cells to grow faster and live longer, potentially leading to more dangerous strains of cancer.
It’s not yet known whether telomerase treatment of humans would extend our lifespans – or lead to dangerous cancers.