An alternative cancer cell nutrition mechanism has been discovered and investigated.

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    A number of experiments conducted by the International team of scientists with the participation of ITMO University employee Alexei Sergushichev led to the conclusion that lung cancer growth can be stopped by depriving the cancer cell of the ability to connect to alternative sources of nutrition. The discovery was based on the hypothesis of the existence of a mechanism that allows cancer cells to change priorities in choosing their energy donors.

    Cancer cell nutrition mechanism


    The nutrient medium that ensures the development of a healthy and cancerous cell is strikingly different. Extremely rapid growth of cancer cells suggests enhanced energy nutrition. The glucose is the best suited for this purpose, the need for which in a cancer cell is tens or even hundreds of times higher than that in healthy cells. There comes a time when the need for glucose in malignant cells begins to exceed the body's ability to accumulate it, which stimulates the cancer cell to search for an alternative donor.

    An international group of scientists consisting of representatives of McGill University in Montreal, ITMO University, the University of Washington in St. Louis and the University of Bristol conducted an experiment in which the reaction of cancer cells of certain species to glucose deficiency in a nutrient medium was studied.

    During an experiment with cells of the most common variety of lung cancer, the so-called. “Non-small cell” cancer (common in 85-90% of the total number of patients), it turned out that at the moment when glucose begins to be in short supply, the cells begin to “develop” the energy resources of another donor, which in this case becomes the amino acid glutamine. Continuing the study of the effect of selective donor change, scientists came to the conclusion that using an enzyme called PEPCK helps to use glutamine as an energy source for cancer cells. Integrating into the metabolism of cells, this enzyme becomes the “bridge” through which glutamine energy is delivered to cancer cells. Thus, scientists were able to find out both the source and the route of delivery of cancer cells energy resources necessary for their growth and survival.

    As a result of further research conducted on laboratory mice and aimed at blocking the enzyme PEPCK, scientists were able to prove the viability of the hypothesis: the growth rate of a cancerous tumor lacking an alternative source of nutrition decreases sharply.

    “Understanding the mechanisms used by cancer cells to provide fast growth rates opens up new possibilities for treating this disease,” says Aleksey Sergushichev, bioinformatics and graduate student at the Department of Computer Technology, ITMO University. “An aimed blow aimed at depriving the cells of their ability to adapt to environmental conditions through metabolic pathways associated with the PEPCK enzyme can be an effective way to treat a number of types of cancer, and in particular one of the most common on the planet - non-small cell lung cancer.”

    Another important conclusion reached by the joint group of scientists was the proof that the lung tissue of cancer patients contains high concentration of PEPCK.

    The results of the studies finally confirmed the fact that in the nutrient medium of the body, cancer cells not only successfully compete in the struggle for the main source of energy - glucose, but also retain the ability to switch to alternative sources of nutrition in case of deficiency.

    “Our work has clearly demonstrated that under stress, cancer cells can use alternative sources of nutrition. This amazing adaptability is part of the mechanism that makes cancer deadly, but at the same time inspires hope for finding effective ways to defeat it. ” - summarizes Russell Jones, professor of physiology at the Center for Cancer Research. Goodman at McGill University.

    The results of the work of the international team are published on the cover of the rating magazine Molecular Cell .

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