{
  "id": 196852,
  "title": "A 'molecular switch' that heals the gut—and that colorectal cancer hijacks to spread",
  "url": "https://urgent.news/2026/08/05/a-molecular-switch-that-heals-the-gut-and-that-colorectal-cancer",
  "topic": "health",
  "section": "Health & Medicine",
  "published": "2026-08-05T22:20:03.000Z",
  "source": {
    "name": "Medical Xpress",
    "slug": "medical-xpress",
    "url": "https://medicalxpress.com/news/2026-08-molecular-gut-colorectal-cancer-hijacks.html"
  },
  "original_language": "en",
  "account": "Scientists have discovered a protein called ZFP36L2, or ZFP for short, which acts as a \"molecular switch\" between the body's damage-sensing system in the gut and the cells' ability to change identities and repair injury. This same family of proteins is also involved in colorectal cancer's ability to spread through the body.\n\nThe human gut is constantly regenerating its lining cells through a process driven by stem cells. These specialized stem cells can both replace lost cells and renew themselves. When too many stem cells are lost due to factors like inflammation or infection, the body activates a backup program that allows mature cells to revert back to a stem cell state to create new cells. However, colorectal cancer cells can hijack this process to support their spread to new organs.\n\nZFP36L2 is responsible for turning off the alarm signal that tells cells to enter a stressed state during injury. By targeting messenger RNAs carrying this alarm signal, ZFP36L2 facilitates the transition back to a stem cell state, allowing the cells to rebuild the damaged tissue. Without ZFP36L2, cells struggle to recover from gut injury and cannot complete their transition back to a stem cell state.\n\nColorectal cancer cells exploit this wound-healing machinery to spread when they break away from the primary tumor and enter a stressed, injury-like state similar to gut cells after damage. When ZFP36L2 is missing in colorectal cancer cells, they are unable to rewind back into a stem cell state and establish new tumors in distant organs.\n\nInterestingly, when ZFP36L2 is lost in primary tumor models, tumors grow more slowly, suggesting that cancer cells depend on ZFP to maintain their stem cell identity. However, in about 5% to 10% of colorectal cancer patients, ZFP is mutated or deleted entirely, causing tumors to make abnormal adaptations and shift into non-intestinal cell identities like neuroendocrine or squamous cells, which are associated with poor treatment outcomes.",
  "summary": "Digestion is hard on the cells that line the human gut, and they are constantly being shed and replaced. This renewal is driven by a population of tireless stem cells. These stem cells can both replace the various types of intestinal cells that have been lost and renew themselves.",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}