Telomeres are known to cause aging, but in cancer cells, they enable infinite division. This article explores the role of telomeres, their abnormal behavior in cancer cells, and how they are being used to treat cancer.
A clue has recently been discovered that could unlock the long-kept secret of aging. Telomeres. Telomeres are believed to be the cause of aging, but their reversal offers hope that they can be harnessed to conquer aging. Telomeres are also responsible for cancer, one of the deadliest diseases that threaten human health. However, the same telomeres that cause aging in humans behave differently in cancer cells. In cancer cells, telomeres do not promote cellular aging. In this article, we’ll take a look at what telomeres are, what the mysterious behavior in cancer cells is and what causes it, and what efforts are being made to use them to fight cancer.
Telomeres are specific sequences of bases that repeat at the ends of DNA strands to compensate for the loss of bases during DNA replication. Our bodies are constantly dividing cells to grow, heal wounds, and maintain the function of our organs. This process always involves replicating DNA so that the two cells that divide have the same DNA. However, due to a malfunction of an enzyme in the DNA replication process, an imbalance occurs that causes one strand of DNA to become shorter. This means that as the cell divides, the DNA strands get shorter and shorter, risking damage to the genetic information. To defend against this, strands called telomeres are present at the ends of DNA. These telomeres are strands of unnecessary sequence repeats that can be removed, preventing important genetic information from being damaged. However, as cells continue to divide, they eventually run out of these telomeres, leading many scientists to believe that they hold the secret to aging.
In cancer cells, however, it’s a different story. Cancer is a disease in which the regulatory mechanisms that normally limit cell growth are not working properly. Cells normally regulate the amount of cell division by sending signals to their neighbors. For example, cells in your body normally divide at a steady rate, and when a wound occurs in a certain area, more cell division occurs to repair the damaged tissue. Cancer cells, however, have this regulatory mechanism broken and divide constantly.
Importantly, cancer cells can divide almost indefinitely. In fact, cancer cells from Henrietta Lacks, who died of cervical cancer in the United States in 1951, were cultured in vitro and are still dividing and are used in many studies. So why aren’t cancer cells affected by the problem of shorter DNA ends? The answer lies in an enzyme called telomerase. This is an enzyme that originally comes into play during the formation of reproductive cells. Gametes are cells that are created through meiosis, the process by which male and female gametes meet and fertilize to create a fertilized egg, which grows to become a baby. The process of meiosis does not change the genetic information, so gametes carry the genetic information of the somatic cell from which they originated. However, the somatic cells may already have shortened telomeres. This is where telomerase comes in.
Telomerase is a type of reverse transcriptase enzyme that lengthens shortened telomeres. Reverse transcription is the process of making DNA from RNA, and telomerase uses a strand of RNA that is complementary to the telomere strand to lengthen the shortened chromosome ends. Normally, this enzyme is not active in somatic cells, but it is active during germ cell development. However, most cancer cells use telomerase to extend their lifespan indefinitely. Studies have shown that telomerase is abnormally active in most cancers. Thanks to this enzyme, cancer cells are able to divide indefinitely and still maintain a telomere structure that does not shorten.
In theory, developing a drug that reduces or eliminates the activity of telomerase in cancer cells could conquer cancer. However, the reality is not so simple. First, telomeres can be renewed by other means, even in the absence of telomerase. For example, by homologous recombination and DNA modification. These methods can either increase the length of DNA or increase the length of telomeres. Another problem is that even if telomere synthesis is prevented, it takes time for telomeres to be completely depleted. In the meantime, cancer cells can continue to divide, and it’s difficult to take appropriate action in the meantime.
Conquering cancer is not a simple problem to solve, which is why researchers are continuing to investigate telomeres in cancer treatment. Since abnormal telomerase activity has been found in about 90% of cancers, it could be an important clue to cancer control. One approach is to remove telomerase and then use the immune system to completely eliminate cancer cells. In this method, proteolytic enzymes are applied to the cancer cells to break down telomerase, and the resulting fragments attach to the surface of the cancer cells and act as antigens. Immune cells recognize this antigen and are then triggered to attack the cancer cells.
Although this treatment has been developed through years of research, it hasn’t yet been applied in practice. This is due to safety concerns. This method can destroy not only cancer cells but also normal cells. Immune cells don’t guarantee perfect accuracy when recognizing antigens, and artificially engineered immune cells are especially prone to problems. Nevertheless, the method is faster and more reliable than direct telomerase degradation, which is why it is being studied.
As you can see, cancer treatment research using telomeres is a trial and error process, but it is moving forward with new advances along the way. In addition to telomeres, other methods such as viruses and light therapy are being studied, and it is predicted that cancer will be completely conquered by 2030 as a result of these efforts. Soon, patients will be free from the pain of chemotherapy and the term “incurable” may become a thing of the past.
