A new study led by Weill Cornell Medicine researchers has revealed that linoleic acid—an omega-6 fatty acid common in Western diets—significantly boosts the growth of triple-negative breast cancer, an aggressive and hard-to-treat form of the disease.
Published March 14 in Science, the study is the first to identify a specific biological mechanism connecting linoleic acid to cancer progression. The findings may open the door to personalized dietary recommendations and targeted drug strategies for patients with this subtype of breast cancer.
Triple-negative breast cancer lacks three key hormone receptors, making it resistant to many standard treatments. The Cornell team discovered that linoleic acid activates a major growth pathway in tumor cells by binding to a protein called FABP5, which is abundant in triple-negative tumors. This interaction triggers the mTORC1 pathway—a key driver of cell growth and metabolism.
In mice fed a diet rich in linoleic acid, tumors grew faster and showed higher activity of both FABP5 and mTORC1. The same markers were elevated in tumor and blood samples from newly diagnosed patients with triple-negative breast cancer.
“This discovery helps clarify the relationship between dietary fats and cancer,” said senior author John Blenis, professor of cancer research at Weill Cornell Medicine. “It sheds light on how to define which patients might benefit most from specific nutritional recommendations.”
Linoleic acid, while essential to human health, has become increasingly prevalent in processed foods due to its presence in seed oils like soybean and safflower oil. Past research had suggested a potential link between high omega-6 intake and cancer, but the evidence remained inconclusive—until now.
The study also hints that FABP5 might be useful as a biomarker, guiding future nutritional or pharmaceutical interventions for triple-negative breast cancer patients. Additionally, researchers found that the same omega-6 signaling pathway may fuel the growth of some prostate cancers, suggesting broader implications across multiple diseases.
“There may be a broader role for FABP5-mTORC1 signaling in other cancer types and even in common chronic diseases such as obesity and diabetes,” said first author Nikos Koundouros, a postdoctoral researcher in the Blenis lab.
The research was supported by the National Institutes of Health and a Charles H. Revson Senior Fellowship in Biomedical Science.
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