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A substance from green tea caused cancer cells to self-destruct

TASS, February 12. The volatile substance from green tea can kill cancer cells by causing them to produce p53 protein molecules. He is responsible for checking the integrity of the genome. This is the conclusion reached by American scientists, whose results were published in the scientific journal Nature Communications.

The p53 gene controls the production of a protein that is responsible for the cell’s self-destruction mechanism in the event that serious damage appears in its DNA. because of mutations in this gene appear many different cancers. Besides, due to of such mutations, the tumor is much better resistant to chemotherapy.

In some cases, the p53 gene remains intact, but its activity is reduced due to mutations in other parts of DNA. These include, for example, the MDM2 gene, which protects healthy cells from accidental death by neutralizing “extra” p53 protein molecules. Scientists are trying to figure out how to reactivate p53 and suppress other genes in the hope that cancer cells will self-destruct.

In a new study, Professor Chunyu Wang of the Rensselaer Polytechnic Institute (USA) and his colleagues found that the substance EGCG (epigallocatechin gallate) can play this role. It is found in green tea leaves and other plant foods. EGCG is a powerful antioxidant that can suppress inflammation in humans and animals.

Experimenting with cultures of cancerous and healthy cells, biologists found that EGCG molecules actively bind to p53. As a result, this protein was activated and the cancer cells were destroyed.

“We found that the p53 protein can bind to the volatile EGCG molecules at the same point where the MDM2 protein is attached to it, which is responsible for breaking down its molecules. As a result, the concentration of p53 in cancer cells increases, and it starts a self-destruction program inside them, ”Wang explained.

Wang and his colleagues believe that, thanks to their work, EGCG can be used as a basis for new types of anti-cancer drugs that can act on even the most resistant types of tumors in which the activity of the p53 protein is maximally suppressed.

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