Cancer cells survive by self-eating
Biologists have found out how the "guardian of the genome" works on cancer cellsRIA News
Scientists from the USA and Israel have discovered features of the mechanism of survival of tumor cells in conditions of insufficient resources associated with the work of the p53 protein responsible for anti-cancer protection, according to an article in the journal Proceedings of the National Academy of Sciences (Ruth Scherz-Shouval et al., p53-dependent regulation of autophagy protein LC3 supports cancer cell survival under prolonged starvation).
The p53 protein, called the "guardian of the genome" by scientists, plays a key role in protecting animal cells from genetic damage. In case of serious breakdowns in the genomic DNA molecule, p53 launches a program of apoptosis – cellular "suicide". In this way, in particular, the body is protected from the occurrence of cancerous tumors in it.
In addition to monitoring the state of the genome, p53 regulates a large number of mechanisms inside living cells, in particular, autophagy – the process of "self-digestion" of unnecessary cellular components. This process is especially important in conditions of starvation of cells, when they have to eat at the expense of "internal reserves".
As previously thought, autophagy plays an important role in protecting the body from the development of cancer, but in some cases this process is used by cancer cells to survive in conditions of insufficient resources.
An international team of scientists from the Weizmann Institute (Rehovot, Israel) and the Institute for Advanced Studies (Princeton, USA) has shown how the p53 protein regulates autophagy in cancer cells, contributing to malignant growth.
Molecular biologists compared the properties of HCT116 rectal cancer cells containing the normal p53 gene and cells of the same line artificially deprived of this gene, depending on the availability of nutritional resources.
As a result, it turned out that p53 regulated the synthesis of LC3 protein, one of the key participants in the autophagy process. To the surprise of scientists, p53, which is considered a transcription factor (a molecule that interacts with DNA and affects the work of genes), in this case modulated the formation of LC3 by interacting with its matrix RNA – the molecular "instruction" for protein synthesis.
"The mechanisms by which p53 maintains homeostasis by autophagy are probably different for different cell types," explains Moshe Oren, the head of the work.
"Our results show that p53 regulates autophagy depending on the availability of nutritional resources of the cell. On the one hand, it contributes to anti-cancer protection. On the other hand, this process can provide selective benefits to cancer cells," says Oren. Which of the alternatives will "outweigh" depends on a combination of various factors, including genetic ones, the biologist adds. This, according to scientists, should be the subject of future research.
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