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Metabolites of pathogenic E. coli – against cancer cells
Cancer cells are not foreign infectious agents, but our own cells, in which the work of genes vital for the normal development and functioning of the body has changed. Proteins-enzymes secreted by a strain of E. coli, which causes diseases of the genitourinary tract, helped to block the work of one of these oncogenes.
The term cancer unites a group of diseases characterized by the rapid growth of abnormal cells that can penetrate into neighboring tissues and often metastasize to other tissues and organs. Oncological diseases are currently one of the main causes of death in the world, and scientists have been investigating the mechanisms of their development for decades in search of ways to prevent and treat them.
Back in the 1970s, so-called proto-oncogenes were discovered, which, as a result of mutation or increased activity, turn into oncogenes indicating malignant cell degeneration and tumor growth.
Proto-oncogenes are usually genes encoding proteins that regulate cell division, growth, and differentiation. For example, the c-MYC gene, discovered in 1982, encodes a protein transcription factor involved in the regulation of the chromatin structure, on which the reading of information from a particular DNA site depends. Thus, this gene is involved in the regulation of the activity of many other genes.
In the cells of most cancerous tumors, the production and, accordingly, the activity of the c-MYC protein is increased. But despite the fact that this gene serves as a potential target for the development of anti-cancer drugs, attempts to use its inhibitors therapeutically have so far failed.
Recently, researchers from Sweden, Germany and Singapore, led by Swedish specialists from Lund University, made an amazing discovery based on the observation that the activity of the c-MYC gene is reduced in children with acute pyelonephritis. It turned out that a uropathogenic strain of E. coli (Escherichia coli) is responsible for this phenomenon.
Article by Butler et al. A bacterial protease depletes c-MYC and increases survival in mouse models of bladder and colon cancer is published in the journal Nature Biotechnology.
The researchers were able to identify the "hero" among the many compounds secreted by this bacterium – it turned out to be the Lon protease enzyme, which destroys the c-MYC protein. The enzyme has successfully worked in human and animal cell cultures infected with E. coli. In an experiment on laboratory mice with c-MYC-dependent bladder and colon cancer, the introduction of this enzyme delayed the development of the tumor and increased the survival rate of animals.
The advantages of using the Lon protein do not end there: it turns out that it works mainly where the c-MYC gene is overactive, which is exactly what distinguishes tumor cells. Due to this "targeting", therapy using this bacterial enzyme can be very effective.
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