The Bacterial Protein promoting Cancer

Viral Oncology: The Bacterial Protein promoting Cancer

DNA K, a protein of the bacterium mycoplasma, interferes with the mycoplasma-infected cell's ability to respond to and repair DNA damage, a known origin of cancer. Little or no mycoplasma DnaK DNA sequences were found associated with the tumor, which was fully developed, suggesting a hit-and-run or hide mechanism of transformation, indicating that the damage is done early, but the protein may not be needed once the cancer cells are formed.

                  Mycoplasmas are a family of bacteria that are associated with cancers, especially in people with HIV. Researchers utilized immune-compromised mice as a model for analyzing the effect of mycoplasma infection on the development of lymphoma. They compared how quickly non-infected immune-compromised mice developed lymphoma compared to mycoplasma-infected immune-compromised mice. The mice were infected with a strain of mycoplasma from an HIV patient. The researchers found that mycoplasma infection caused the mice to develop lymphoma earlier in life than non-infected immune-compromised mice and that some, but not all, of the cancer cells had bacterial DNA. Finding only a small amount of bacterial DNA in the cancer cells suggested that the infection did not have to persist to trigger cancer.

               We focused on a protein called DnaK, which is part of a family of proteins that function as a 'chaperone' for other proteins protecting them from damage or helping them to fold, However, in this case, DnaK reduces the activity of important cellular proteins involved in DNA repair and anti-cancer-activities, such as p53. Thus, cells infected with mycoplasma would not be able to properly repair damaged DNA, thus, potentially increasing the risk for cancer development.

                   The scientists noted that the bacteria can release DnaK and the DnaK enters nearby uninfected cells. The study also demonstrates that by reducing p53, DnaK can also reduce the efficacy of anti-cancer drugs. Thus, mycoplasma infection could not only trigger events leading to the accumulation of DNA damage and oncogenesis in infected cells, but also trigger cancer-causing events in nearby uninfected cells that took up DnaK released from infected neighboring cells.

                 We analyzed the amino acid sequences of DnaK from many bacteria and found that the DnaK proteins from bacteria associated with cancer grouped together were different DnaK sequences from bacteria that are not associated with cancer; this raises the possibility that other bacteria have the same cancer-promoting ability.