Researchers Uncover Hidden Aging Program in Gut that Increases Cancer Risk

Researchers in the life sciences have identified a hidden aging program in the gut that may contribute to the risk of colorectal cancer.

Despite the gut's constant regeneration, stem cells accumulate molecular changes related to aging, subtly altering how genes are activated and deactivated. An international team of researchers has found a clear pattern of this 'epigenetic imbalance' that appears in both aging intestines and the majority of colon cancers. Some regions of the gut age faster than others, creating a mosaic of weakened tissues that are more prone to degeneration.

Encouragingly, studies indicate that this process can be slowed and partially reversed by restoring iron levels or through key cellular signaling. The research team, led by Professor Francesco Neri from the University of Turin, identified a process called 'ACCA drift' (Associated with Aging and Colorectal Cancer), which is a gradual shift of epigenetic markers that becomes more pronounced as people age.

The genes most affected by this process are those that help maintain the normal balance of tissues. When these genes are altered, the gut's ability to repair itself begins to weaken. Studies have shown that this drift pattern occurs not only in aged intestinal tissue but also in nearly all analyzed colorectal cancer samples. This overlap suggests that aging stem cells may create conditions conducive to cancer development.

Another interesting aspect is that aging does not affect the gut uniformly. Consequently, some chromosomes remain relatively healthy, while others become more prone to producing damaged cells, thereby increasing the chances of cancer development. Researchers also found that iron loss disrupts DNA repair and that age-related inflammation in the gut exacerbates the issue.

However, through laboratory experiments, researchers have managed to slow down or partially reverse this epigenetic drift by restoring iron uptake or directly stimulating Wnt signaling. These advancements suggest that epigenetic aging need not be a fixed and final state.