A new study suggests that bacteria inside pancreatic tumors may actively drive cancer growth in pancreatic ductal adenocarcinoma (PDAC). Researchers found that Enterococcus faecalis is enriched within tumor tissue and can invade pancreatic cancer cells, where it survives and alters cell behavior.
In laboratory experiments, exposure to this bacterium increased cancer cell growth, division, migration, and invasion. It also raised levels of key cancer-related markers linked to tumor aggressiveness.
The study identified a specific mechanism behind this effect. The bacteria activate Toll-like receptors (TLR2, TLR4, and TLR6) in cancer cells, leading to increased reactive oxygen species (ROS). This, in turn, triggers activation of EGFR signaling and downstream cancer-promoting pathways such as PI3K-Akt and MAPK. The infection also stimulates the release of inflammatory and tumor-promoting cytokines, creating a feedback loop that supports tumor growth.
In mouse models, tumors exposed to E. faecalis grew faster and were larger than controls.
Researchers suggest that targeting these bacteria-related pathways could offer new treatment strategies for pancreatic cancer.