Profitable competition
Mutant cells do not allow each other to turn into a tumor
Kirill Stasevich, Science and Life (nkj.ru )
Malignant tumors arise due to mutations that allow cells to divide uncontrollably. These mutations appear both due to external factors, such as carcinogenic substances that we eat and inhale, and for natural internal reasons. Our cells are regularly updated, new ones come in place of the old ones, and new ones are taken from progenitor stem cells, which retain the ability to divide for a very long time. But when dividing, molecular machines that double DNA inevitably make mistakes that remain uncorrected and gradually accumulate. Some researchers believe that cancer mutations arise for the most part just because of inaccurate DNA copying.
Some mutations appear in our youth (as in the uterus, for example), and with age their number increases tenfold. However, they do not always lead to something bad. Researchers from the Sanger Institute believe that cancer mutations remain safe due to competition between mutant cells.
A mutation in a stem cell can get (and often does) into an oncogene – that is, into a gene that, for example, controls cell division, but which normally retains a connection with reality, that is, perceives restrictive signals from the external environment, from other cells, from other genes of the same cell, etc. But after mutation, such a gene becomes a little less controllable, and now the progenitor stem cell begins to divide a little faster than a normal stem cell. Cancer will not start with one mutation, but if a mutant cell breeds many descendants, then it is more likely that a couple more will be added to this first mutation, and the cells will begin to divide in a cancerous way.
But cells do not exist in the tissue by themselves, but surrounded by many other cells. And mutations can also appear in them, which accelerate their division, making it a little less controllable. And if some mutants collide with others who have the same competitive advantages, they will start interfering with each other, and as a result, no one will divide faster and no tumor will appear. There is not enough space in our tissues, so the cells have to coordinate their interests with each other.
The researchers tested this hypothesis in experiments with mice in which esophageal epithelial cells were specially forced to mutate (esophagus and skin are two organs in which by middle age most cells already carry certain mutations). Mutations were very carefully searched out in mouse cells and compared these mutations with how successfully mutant cells of the same genus occupy the territory and how their success correlates with their neighbors. An article in Nature Genetics (Colom et al., Spatial competition shapes the dynamic mutational landscape of normal esophageal epithelium) states that mutant clones really held each other back, so that in the end all cells divided at a normal rate. Of course, if mutations appear in some cells that immediately give a strong advantage, then it will not be possible to balance them with other cells, and most likely a tumor will begin to develop.
The authors of the work do not yet know exactly how mutant cells restrain each other. But if we understand what signals they send to each other, which molecules they use, then we ourselves can use these same signals to suppress the growth of real cancer cells.
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