12 April 2021
Inflammation promotes colorectal cancer
Published online 22 August 2012
Chronic inflammation has been identified as a risk factor for several types of cancer, including colorectal cancer (CRC). A recent study suggests that acute inflammation creates conducive conditions for cancer cells to develop.
Janelle Arthur from the University of North Carolina in Chapel Hill, United States, led a team of researchers including Turki Abujamel from the King Abdulaziz University in Saudi Arabia, studied the effect of inflammation on the development of CRC in mice and publish their findings in Science.
They compared wild-type mice with interleukin-10-deficient mice, which are susceptible to inflammation, in the presence and absence of a colon-specific carcinogen polyketide synthase (pks).
With the introduction of pks, 60–80% of the interleukin-10-deficient mice developed tumours while none of the wild-type mice did. Repeating the process without pks reduced the growth of cancer, but did not dampen inflammation.
"This demonstrated that while inflammation was required for tumorigenesis in this model, it was not sufficient," says Arthur.
"The microbial pks genotoxic island promotes the development of cancer independently of intestinal inflammation."
The researchers suggest that inflammation has a twofold approach in promoting the conditions for CRC development. On one hand, it targets the microbiota, which is formed of trillions of bacteria living in the human colon and increases the levels of genotoxic bacteria such as adherent-invasive Escherichia coli.
Simultaneously, inflammation thwarts production of protective mucins, making it easier for harmful bacteria to stick to the mucosa that coats colon cells. This increased contact between bacteria and epithelial tissues creates a better conduit for bacteria to transmit tumorigenetic substances.
"The next steps we may be taking are to further explore the mechanism by which pks induces genotoxicity," adds Arthur.
- Arthur, J. C. et al. Intestinal Inflammation Targets Cancer-Inducing Activity of the Microbiota. Science doi:10.1126/science.1224820