As we age, changes in our DNA can influence our health. A recent study has found that these changes, particularly in gut stem cells, may play a role in increasing our risk of colorectal cancer. This process is called Aging and Colon Cancer-Associated (ACCA) drift. It involves modifications to DNA that can turn genes on or off without altering the actual DNA sequence.
The researchers discovered that this drift leads to the silencing of genes that typically help prevent tumor growth. As a result, the risk of cancer builds up in the cells of our gut long before any visible tumors emerge. “We see a pattern of epigenetic changes that grows more noticeable with age,” said Francesco Neri, a molecular biologist from the University of Turin.
Starting from what we already knew—epigenetic changes are linked to cancer and that the risk of colorectal cancer increases as we get older—the research examined tissue samples from healthy colons and cancerous tumors. They found similar patterns of gene silencing, suggesting a shared underlying mechanism.
Experiments using mouse models and lab-grown miniatures of the intestine confirmed that this drift is unique to the gut. The researchers focused on tiny pockets in the gut lining called intestinal crypts. These crypts contain stem cells that renew the intestinal lining. The ACCA drift begins in these stem cells and spreads as they divide.
What’s happening? Increased inflammation, fewer growth signals, and low iron levels in the stem cells disrupt methylation processes. This dysfunction leads to gene deactivation, potentially enabling cancer to form. “Over time, more areas of tissue develop an older epigenetic profile,” said Anna Krepelova, also from the University of Turin. “These regions can grow over the years as crypts divide.”
A lack of iron in cells leaves behind faulty DNA markings. As stem cells multiply, patches of tissue with a higher risk of cancer gradually expand throughout the gut.
Recent research shows that nine out of ten colorectal cancer cases are preventable through lifestyle changes, including diet and exercise. Addressing inflammation and maintaining balanced iron levels could be crucial in managing this risk.
Interestingly, the study found that boosting iron uptake or restoring specific growth signals could slow or even partly reverse these epigenetic changes in lab-grown tissues. “This suggests that epigenetic aging isn’t a permanent state,” Krepelova noted. We now have potential ways to intervene in the aging process at a molecular level.
Understanding these mechanisms and the influence of diet and inflammation may lead to effective strategies for reducing colorectal cancer risk as we age. For further reading, you can explore the study published in Nature Aging here.
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