A mouth bacterium that both promotes and fights cancer
Fusobacterium nucleatum is a bacterium that normally lives in your mouth but is also found deep inside tumors. Scientists have long known it can fuel cancer.
The relationship between bacteria and cancer is more complicated than previously assumed. Fusobacterium nucleatum — a common inhabitant of the gums and a familiar culprit in gum disease — has in recent years been repeatedly found inside colorectal tumors and certain head and neck cancers. In that context, it appeared to feed the cancer: it stimulated tumor growth and helped cancer cells evade the immune system. But that turned out not to be the full picture.
An unexpected contact with immune cells
Researchers publishing in eLife discovered that a specific protein on the surface of Fusobacterium, called RadD, can directly bind to a receptor on natural killer cells — NK cells, a type of white blood cell specialized in killing cancer cells and virus-infected cells. That receptor is called NKp46. The binding activates the NK cell — it becomes sharper, more aggressive toward tumor cells.
Analysis of cancer patient data revealed something striking: in patients with head and neck cancer, the presence of Fusobacterium combined with high NKp46 expression was associated with better survival outcomes. In other words, the same bacterium that strengthens cancer in some contexts can, in other contexts, sharpen the immune system to fight it.
Context determines everything
How can one bacterium have such opposing effects? The answer likely lies in the environment: the type of tumor, the patient’s immune status, the presence of other microorganisms, and the expression of specific receptors in the tumor tissue. Biology rarely works in binary terms. Bacteria are neither heroes nor villains — they respond to their environment and activate different pathways depending on what is present nearby.
The practical implications are twofold. On one hand, this suggests that simply eliminating Fusobacterium in cancer patients may not be a good idea — it could also have protective effects. On the other hand, it opens a new avenue: if RadD-NKp46 binding activates NK cells, synthetically mimicking that interaction could be a way to mobilize the immune system against tumors. That remains speculative, but the molecular foundation is now established.