Some rodents have a mysterious defense mechanism against cancer, which allows them to live (by the standards of such tiny creatures) happily ever after. And if humanity wants to learn how to deal with cancerous tumors and metastases, it should look for a recipe, say, from ordinary proteins
So say biologist Vera Gorbunova and her colleagues from the University of Rochester.
“We haven’t come across this antitumor mechanism until now, because it does not exist in the two species that are most commonly used for cancer research: in mice and in humans,” Gorbunova says. - Mice are small and do not live long, people are large and live much longer. And this mechanism, it seems, exists only in small and at the same time long-lived animals."
Scientists made their discovery by studying the expression of genes that are responsible for the work of the telomere enzyme in cells - protective sites at the ends of chromosomes, which are shortened with each cycle of cell division.
Therefore, the high activity of this enzyme (regulated by certain proteins - the catalytic components of telomerase) prolongs the time during which the cell retains the ability to divide. This promotes tissue self-healing in case of damage, but, like a price, significantly increases the risk of cancer.
Biologists also associate the life span of living beings and the risk of mutations with the gradual shortening of telomeres.
But this process is just one of many factors: the genetic mechanisms of aging, as well as age-related changes in metabolism, are just beginning to reveal their secrets. And the connection between telomeres and tissue repair is quite ambiguous.
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| Telomeres at the ends of chromosomes. These sections of DNA protect the genetic information of the cell, but with each division they do not fully reproduce (illustration from the site wikimedia.org). |
Previously, scientists believed that telomerase expression was determined by the lifespan of a species.
In creatures living longer than 70 years, in old age, the chance of the appearance of cancer cells increases, and then, they say, genes begin to suppress the activity of the enzyme, protecting the body as much as possible from cancer, but, alas, without thereby prolonging the life of the earthly existence (if at the end of our life, telomerase activity was not suppressed, we would get cancer much more often).
However, Gorbunova's previous work showed that, in fact, the expression of telomerase and its suppression in individuals "aged" well correlates not with life expectancy, but with body weight. There is logic in this. The more cells in the body, the higher the likelihood that one of them will sooner or later become cancerous.
A new study by scientists from the University of Rochester has revealed even more interesting details "from the life of telomerase," using the example of rodents.
Why exactly them? The fact is that different types of rodents occupy a very wide range in body weight, at the same time, they are all related animals, which makes it possible to more correctly compare their genes.
| Weight and lifespan of some rodents. As you can see, there is no unambiguous correlation between the one and the other. There is only an approximate pattern (harder - longer) and a number of interesting exceptions to this rule (illustration from the site rochester.edu). |
So it turned out that the enzyme is active throughout life in small rodents, but not in large ones.
Further, even stranger differences emerged. For example, mice with their active telomerase do not live long, and proteins (also with this "switched on" enzyme) - a quarter of a century. At the same time, squirrel populations do not die out from cancer at all: tailed nut lovers happily avoid any form of it.
With mice, everything is more or less clear - these animals can get cancer, but for them such a chance is not so important - the cat will eat earlier. But being able to heal wounds can be critical.
In proteins, the researchers explain, there is a kind of compensation mechanism that prevents the development of cancer, despite constantly active telomerase. And this "invention" is used not only by proteins. Hairless mole rats, chipmunks, muskrats and chinchillas also distinguished themselves.
(Details of the discovery can be found in a university press release and in an article by the study authors in the journal Aging Cell.)
What is this mechanism?
Gorbunova believes that proteins and some of their other relatives have developed strict control over the functions of cells. The latter can themselves "understand" whether the division is appropriate or inappropriate at a given moment, that is, they distinguish between healthy reproduction and unrestrained reproduction - cancer.
Cells in proteins somehow prevent their division, and only when it is really necessary. Biologists from Rochester suggest that cells in long-lived but small rodents are very sensitive to signals from surrounding tissues, which allows such cells to "decide" whether to divide or not.
Vera and her colleagues hope to discover and explain this defense mechanism against cancer. And there, perhaps, there will be a way to include it in a person.