Bacteria could have a bigger involvement in cancer than scientists may have realized, according to recent research.
A study from the University of Maryland School of Medicine in Baltimore has uncovered a type of bacterial infection that can disrupt DNA repair in cells, which is a known cause of cancer.
The same type of infection could also weaken the effect of some anticancer drugs, says the PNAS report on the findings.
“Currently,” comments senior study author Robert C. Gallo, who is a professor of medicine and director of the university’s Institute of Human Virology, “approximately 20 percent of cancers are thought to be caused by infection, most are known to be due to viruses.”
The team began by investigating infections by a family of tiny bacteria that go by the name of mycoplasmas.
These bacteria “are associated with cancers, especially in people with HIV,” explains Prof. Gallo, who was one of the scientists who discovered that HIV is the virus that causes AIDS.
Mycoplasmas are among the smallest “free-living microorganisms.” They do not have a cell wall and, for a long time, scientists thought that they were viruses.
The tiny bacteria contain a protein called DnaK that the researchers decided to focus on “because of its ability to interact with proteins.”
DnaK is a “chaperone protein” that protects other proteins from damage and ensures that they function properly by helping them to fold.
The team’s efforts uncovered two main links between DnaK and cancer.
They revealed that DnaK from mycoplasmas “interacts with and reduces the activities of human proteins” that are important for DNA repair.
Also, it appears that DnaK weakens the effect of certain drugs that aim to boost the activity of the natural anticancer protein p53.
DnaK reduces p53 by binding to an enzyme called USP10 that helps to regulate p53.
In their investigations, the researchers observed how quickly lymphoma developed in two groups of mice with compromised immune systems.
They infected one group of mice with a mycoplasma strain from a person with HIV.
The results showed that lymphoma developed more quickly in the mycoplasma-infected immune-compromised mice than their non-infected counterparts.
In addition, some of the cancer cells, but not all of them, contained DNA from the bacteria.
The researchers suggest that this means that the infection does not have to persist to be able to trigger cancer.
It seems that mycoplasma release DnaK and that this can enter uninfected cells that are nearby and trigger events that can lead to cancer in those cells.
Finally, an analysis of amino acid composition revealed differences between DnaK proteins from cancer-associated bacteria and bacteria that researchers have not associated with cancer.
This could mean that there are other bacteria with a similar ability to promote cancer.
Prof. Gallo suggests that their research “changes how we need to think about infection and at least some cancers.”
“Our work provides an explanation for how a bacterial infection can trigger a series of events that lead to cancer.”
Prof. Robert C. Gallo