July 21 (UPI) -- The bacteria in the mouth that causes tooth decay might also help colon cancer spread to other organs in the body, according to a study published Tuesday by the journal Science Signaling.
The bacteria, called Fusobacterium nucleatum, travels through the bloodstream to other organs in the body, leading to infections and allowing cancer cells to migrate or metastasize, researchers at Virginia Tech University said.
"Oral infections that cause inflammation of the gums have been reported as risk factors for systemic infections, cardiovascular disease, adverse pregnancy outcomes, diabetes, cancer and Alzheimer's disease," study co-author Daniel J. Slade told UPI.
"People can potentially avoid infections by maintaining good oral health, which could in turn keep the levels of Fusobacterium nucleatum in the dental plaque under control, and treating infections that lead to tooth decay is a critical preventative measure to stop bacteria from entering the bloodstream," said Slade, an assistant professor of biochemistry at Virginia Tech.
These bacteria, however, don't cause colon cancer, which has been linked with poor diet, smoking and heavy drinking, as well as a family history of the disease. Rather, they play a role in "tumor progression," Slade said.
More than 100,000 Americans will be diagnosed with colon cancer in 2020, according to the American Cancer Society.
More than 90% of deaths linked with the disease are caused by "non-primary tumors or sites that have metastasized to somewhere else in the body," Slade said.
Using cancer cell cultures, he and his team found that bacteria that originates in the mouth sticks to and enters disease cells in the colon.
This causes the cancer cells to release two proteins -- IL-8 and CXCL1 -- that help the human immune system fight infections, the researchers said.
These proteins send signals out to cancer cells, immune cells and various other cell types that surround a tumor, causing them to grow and spread, they said.
Identifying the role Fusobacterium nucleatum plays in colon cancer spread might assist in development of drug therapies for the disease, Slade and his colleagues said.
New treatments could seek to block secretion of the immune cells IL-8 and CXCL1 to combat cancer metastasis, they said.
It's also possible antibiotics to designed to kill the bacteria could disrupt the process, but they also might target so-called "good bacteria" in the mouth and digestive tract that help the body process food, researchers said.
"Multiple drugs are in clinical trials to block the human receptors that respond to IL-8 and CXCL1, and these could potentially combat how bacteria accelerates cancer," Slade told UPI.
"In addition, there is the potential for developing new molecules that could block the docking between the bacteria and human host to interrupt these processes," he said.
