Scientists discovered that eating a high-fat diet may make it harder for your body’s immune system to fight colorectal cancer. The research shows that a high-fat diet triggers a chain reaction in cancer cells that helps them hide from immune cells called T cells, which normally attack cancer. When mice with colorectal cancer ate a high-fat diet, their cancer grew faster and didn’t respond as well to immune-boosting treatments. The study found that blocking a specific protein involved in this hiding process restored the immune system’s ability to fight the cancer. This discovery could help doctors develop better cancer treatments for people who are overweight or obese.

The Quick Take

  • What they studied: How eating a high-fat diet affects cancer’s ability to escape the immune system and whether blocking certain proteins can help the immune system fight back
  • Who participated: Laboratory mice with colorectal cancer that were fed either normal diets or high-fat diets, with some receiving immune-boosting cancer treatment
  • Key finding: Mice on high-fat diets developed tumors that grew faster and resisted immune treatment better than mice on normal diets. The high-fat diet activated a protein called STAT3, which turned on a cancer-hiding protein called CD155, allowing tumors to escape immune attack.
  • What it means for you: If you’re overweight or obese, eating a healthier diet with less fat may help your immune system fight colorectal cancer more effectively. However, this is early research in mice, and more studies in humans are needed before making medical decisions. Talk to your doctor about diet and cancer risk.

The Research Details

Researchers used laboratory mice with colorectal cancer to study how diet affects cancer growth and immune response. They created three groups of cancer cells: normal cells, cells with extra copies of the CD155 hiding protein, and cells with reduced STAT3 protein. Each group was tested in mice eating either a normal diet or a high-fat diet, and some mice received an immune-boosting drug called anti-PD-L1 that helps the immune system attack cancer.

The scientists measured tumor growth, counted different types of immune cells in the tumors, and examined which genes were turned on or off. They used special techniques to confirm that the STAT3 protein directly controlled the CD155 gene, showing the exact mechanism of how high-fat diet promotes cancer immune evasion.

This type of controlled laboratory study allows researchers to test specific causes and effects that would be difficult or unethical to study directly in humans. The findings provide a foundation for understanding how diet might influence cancer treatment effectiveness.

Understanding the exact mechanism—the step-by-step process—of how high-fat diets help cancer hide is crucial for developing new treatments. By identifying the STAT3 and CD155 proteins as key players, doctors might be able to create drugs that block this hiding process, making existing cancer treatments work better. This is especially important because obesity is becoming more common, and many cancer patients are overweight.

This is laboratory research using animal models, which is a reliable way to study disease mechanisms but doesn’t directly prove the same effects occur in humans. The study used multiple approaches (flow cytometry, Western blotting, and chromatin immunoprecipitation) to confirm findings, which strengthens confidence in the results. However, mice don’t always respond to treatments the same way humans do, so human studies are needed to confirm these findings apply to people.

What the Results Show

The main discovery was that mice eating a high-fat diet developed colorectal tumors that grew significantly faster than mice on normal diets. More importantly, the immune-boosting drug (anti-PD-L1) that normally helps fight cancer didn’t work as well in mice on high-fat diets.

The researchers identified the mechanism: high-fat diet activated a protein called STAT3 inside cancer cells. This activated STAT3 then turned on production of another protein called CD155, which acts like a shield that helps cancer cells hide from immune cells called CD8+ T cells. At the same time, the high-fat diet increased the number of regulatory T cells—immune cells that actually suppress anti-cancer immunity.

When the scientists blocked STAT3 in cancer cells, the CD155 shield disappeared, immune cells could attack the cancer again, and the anti-PD-L1 drug worked much better. This showed that the STAT3-CD155 pathway is the critical link between high-fat diet and cancer immune evasion.

The study also found that cancer cells with extra CD155 protein were better at hiding from the immune system and grew faster, even without a high-fat diet. This confirms that CD155 is a key player in cancer’s ability to escape immune attack. Additionally, the research showed that the high-fat diet’s effects on immune suppression were reversible—when STAT3 was blocked, the immune system regained its ability to fight cancer, suggesting potential treatment strategies.

Previous research has shown that obesity impairs cancer immunotherapy, but the exact mechanisms were unclear. This study provides a specific molecular explanation—the STAT3/CD155 pathway—that connects diet to immune suppression. The findings align with other research showing that metabolic stress from obesity affects immune cell function, but this is the first to clearly demonstrate this specific pathway in colorectal cancer.

This research was conducted entirely in laboratory mice, not humans, so results may not directly apply to people. The study used a specific type of colorectal cancer model, so findings might differ for other cancer types or subtypes. The research doesn’t address other factors that influence cancer and immunity, such as exercise, sleep, stress, or other dietary components beyond fat content. Additionally, the study doesn’t examine how long-term dietary changes might affect the STAT3/CD155 pathway or whether the effects are reversible through diet modification alone.

The Bottom Line

Based on this research, maintaining a healthy weight and eating a diet lower in fat may help your immune system fight colorectal cancer more effectively, especially if you’re receiving immunotherapy. However, this is early-stage research in animals. Current evidence suggests that a balanced diet with appropriate fat intake is part of overall cancer prevention and treatment support. Discuss specific dietary recommendations with your oncologist or registered dietitian, as individual needs vary based on your health status and treatment plan.

This research is most relevant to people with colorectal cancer, especially those who are overweight or obese, and their doctors. It’s also important for people at high risk for colorectal cancer due to family history or other factors. People considering immunotherapy for cancer should discuss diet with their medical team. However, this doesn’t mean people without cancer need to make immediate changes based on this single study—it’s one piece of evidence among many about diet and health.

If dietary changes were made, it would likely take weeks to months to see effects on immune function, and longer to see impacts on cancer growth. This is not a quick fix. Cancer treatment and prevention require sustained lifestyle changes over time, combined with medical care.

Want to Apply This Research?

  • Track daily fat intake (grams) and weight weekly. Users can set a target fat intake based on their doctor’s recommendations and monitor whether staying within that target correlates with energy levels and treatment side effects.
  • Users can log meals and receive real-time feedback on fat content, helping them gradually reduce high-fat foods. The app could suggest lower-fat alternatives and track progress toward weight loss goals if recommended by their healthcare provider.
  • Create a dashboard showing 4-week trends in fat intake, weight, and any cancer-related symptoms or treatment response markers that the user tracks with their doctor. Include reminders to discuss dietary changes and their effects at medical appointments.

This research is based on laboratory studies in mice and has not been tested in humans. It should not be used to make medical decisions without consulting your healthcare provider. If you have colorectal cancer or are at risk for it, discuss diet, weight management, and treatment options with your oncologist or gastroenterologist. This information is educational and does not replace professional medical advice, diagnosis, or treatment.