Study reveals how dietary fat can influence cancer growth

Study reveals how dietary fat can influence cancer growth
Jonathan Holloway President of Rutgers University — Rutgers University Official Website
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Professor Estela Jacinto from Rutgers Robert Wood Johnson Medical School has been at the forefront of research into the pathways responsible for human cell growth and metabolism for over 20 years. Recently, Jacinto elaborated on new findings published in the journal Science regarding the role dietary fats play in cancer growth.

Researchers have identified omega-6 linoleic acid, an essential fatty acid found in many Western diets, as a direct activator of the mTORC1 pathway—a critical route for cell growth. This activation relies on the protein FABP5. “Researchers discovered that an essential fatty acid called omega-6 linoleic acid, which we can only get by eating it, directly activates a central growth pathway in our cells called mTORC1,” explained Jacinto. “When omega-6 linoleic acid binds to FABP5, it activates mTORC1, which then drives cell growth and proliferation.”

This research underscores the importance of understanding how dietary fats like omega-6 and omega-3 fatty acids impact cellular processes. In particular, excessive omega-6 intake can overly stimulate mTORC1, potentially leading to deregulated cell growth. “The research shows that omega-6, but not omega-3 or its derivatives, activates the mTORC1 growth pathway,” Jacinto noted. “This strengthens the notion that excess omega-6 can potentially have adverse effects by overstimulating mTORC1 and, consequently, deregulating cell growth.”

The study also focuses on cancer, especially breast cancer. FABP5, the protein that facilitates omega-6’s effect on mTORC1, is more prevalent in certain cancers, including triple-negative breast cancer. Experiments with mice demonstrated that diets rich in omega-6 led to increased tumor growth in these cancer forms. “This suggests that tumors with abundant FABP5 may preferentially use dietary omega-6 to fuel their growth,” Jacinto said.

For cancer patients, particularly those with high FABP5 levels, the findings suggest restricting omega-6 intake as a potential treatment strategy. Jacinto proposed, “The research points to a possible therapeutic strategy that combines targeting both mTOR and FABP5, along with dietary omega-6 restriction.”

This research holds the potential to influence dietary guidelines, promoting a balanced intake of omega-6 and omega-3 fatty acids. “A balanced intake of omega-6 and omega-3 fatty acids is already gaining traction in promoting healthy immunity,” mentioned Jacinto. The emphasis on balance rather than elimination highlights the essential nature of omega-6 in diets.

The next phase of research will focus on targeting FABPs and mTOR for cancer treatment, exploring the interactions between dietary fats and cellular metabolism, and setting the groundwork for personalized cancer therapies. “Future research should investigate how excess dietary fat reprograms both cellular and whole-body metabolism,” Jacinto explained, aiming for a better understanding of cancer initiation and progression.

Jacinto concluded by highlighting the significance of these discoveries in cancer metabolism, emphasizing the need for therapeutic interventions that integrate dietary considerations. The link between omega-6 linoleic acid and the growth of cancer cells offers a promising avenue for new treatment strategies.



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