Aging – protection from cancer
Biologists have uncovered a new link between cancer and aging
The search for new cancer drugs unexpectedly revealed an amazing link between aging and cancer, once again indicating that old age is a protective mechanism against the development of tumors, according to an article published in the Journal of Biological Chemistry (Selvam et al., Balance between senescence and apoptosis is regulated by the telomere damage–induced association between p16 and caspase-3).
"We are very pleased that we were able to find at least one defense mechanism that reveals the link between aging and the risk of getting cancer. We hope that eventually we will be able to solve both problems – to slow down aging and prevent the development of cancer," he said Besim Ogretmen from the Medical University of Southern California in Charleston (USA).
Embryo cells and embryonic stem cells are virtually immortal from the point of view of biology: they can live almost indefinitely in an adequate habitat and divide an unlimited number of times. In contrast, adult body cells gradually lose their ability to divide after 40-50 division cycles, entering the aging phase, which presumably reduces the chances of developing cancer.
Why do cells do this? As scientists believe today, in this way cells protect themselves and the body as a whole from the development of cancer, stopping division at a time when the probability of mutations in their genome reaches a certain critical point. The decrepitude of the body, in turn, is a side effect of this process associated with the accumulation of "aged" cells in organs.
Ogretman and his colleagues found further confirmation of this hypothesis by observing the life and death of certain types of cancer cells extracted from the lungs of humans and rodents. Their common feature was that they had damaged the CDKN2A gene, which is responsible for the assembly of molecules of a special protein p16, which plays the role of a kind of "division counter" and "inspector" of DNA integrity.
As scientists used to believe, with each division, p16 checks the length of the end sections of chromosomes, the so-called telomeres, and forces the cell to self-destruct or "retire" if they have become short enough.
Experiments with cancer cells have shown that this is not entirely true. As Ogretman and his colleagues discovered, p16 actually performs only one of these operations – puts the cell into "sleep mode" if its telomeres are reduced to critically small sizes, and prevents the inclusion of chains of enzymes responsible for its self-destruction.
Interestingly, a similar reaction can be caused in cancer cells if the protein SphK2, responsible for repairing telomeres, is blocked and a large number of p16 molecules are introduced into the nutrient medium. Similar processes, according to scientists, can cause accelerated aging in some people and other developmental disorders.
According to Ogretman, the substance ABC294640 created by them, which blocks the work of SphK2, is already undergoing the second phase of clinical trials as a drug capable of selectively destroying cancer cells that contain abnormally few p16 protein molecules.
This drug compares favorably with chemotherapy in that it will not kill "normal" cells, since they all contain a sufficient amount of p16 in order to prevent their mass death. Further development of such drugs, as the biologist hopes, will help us prolong our lives without increasing the likelihood of developing cancer.
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