Protein that protects cells from viruses turned out to be an assistant to the tumor

(ORDO NEWS) — Normally, APOBEC3G proteins attack the genome of HIV and other retroviruses, but cancer cells use this mechanism to their advantage – and to the detriment of the body.

Being active in the tumor, the same proteins increase the frequency of mutations, making the neoplasm more dangerous and difficult to treat.

HIV and other retroviruses contain their genetic information not in the form of DNA, but in the form of related RNA molecules.

One of the means of protection against them is the APOBEC3G proteins, which attack these chains by chemically modifying certain links, cytidine (C) nucleoside residues.

This disrupts the work of the virus genome and prevents its reproduction. Therefore, for example, only HIV strains that have a special protein factor that neutralizes APOBEC3G can reproduce effectively.

The cells of the body themselves have to restrain the violent activity of APOBEC3G. How exactly they protect their own DNA from attacks by these proteins is unknown.

However, in cancer cells, these mechanisms seem to work less well, allowing APOBEC3G to act and increasing the mutation rate. This, in turn, increases the danger and risk of tumor metastasis.

Bishoy Faltas and colleagues investigated the role of APOBEC3G in tumor development in bladder cancer using laboratory mice.

Previously, the APOBEC gene, similar to our APOBEC3G, was knocked out (disabled) in rodents.

At the same time, the human variant of APOBEC3G was introduced into the genome of some animals. Finally, they were exposed to chemical carcinogens that stimulate the development of bladder cancer.

Indeed, it turned out that in mice that worked with APOBEC3G, the disease developed significantly more often (in 76 percent of cases) than in animals without working APOBEC and APOBEC3G (53 percent).

Moreover, over the next 30 months, all mice in which these genes were not active survived, while a third of the carriers of human APOBEC3G died. Scientists have shown that mutagenic proteins are located directly in the nuclei of these cells.

Tumors from these rodents carried twice as many mutations as those without APOBEC3G. These mutations have been associated with modifications to cytidine.

Comparing their set with data from The Cancer Genome Atlas database, the authors of the study were convinced that they are widespread in patients with bladder cancer, making the course of the disease worse and reducing the chances of recovery.

All this confirms that cancer cells are able to use the APOBEC3G proteins, which normally protect us from viruses, to their advantage.


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