A study has discovered a method through which obesity affects the ability of some mouth cancers to evade the immune system. A team from the University of Michigan Rogel Cancer Center and School of Dentistry led by Yu Leo Lei, D.D.S., Ph.D. According to this study published in Cell Reports, obesity helps create a kind of tumor microenvironment that promotes tumor growth. A link between saturated fatty acids, the STING-type I interferon pathway, and NLRC3 explains how this occurs.
“We tend to think about increased risks of gastrointestinal tumors, breast cancer, pancreatic cancer, and ovarian cancer when it comes to obesity,” said Lei, an immunologist pathologist and lead author of the study. “Several recent prospective cohorts involving millions of individuals from several continents have revealed a previously unappreciated association between obesity and oral cancer risks.”
“Myeloid cells from obese mice were insensitive to STING agonists and more suppressed T cell activation compared to myeloid cells from lean hosts,” Lei explained. This property caused the loss of immune subsets that were crucial for antitumor immunity in the tumor microenvironment.
The team found that saturated fatty acids can block the STING pathway, which is induced by cytosolic DNA and promotes the maturation of antigen-presenting cells, by inducing a protein called NLRC3.
Lei says this is the first study to demonstrate a mechanistic link between obesity and immune evasion in oral cancer. “We’re excited about the translational implications,” he continued.
Obesity is a common comorbidity in cancer patients. Two recent studies found that oral cancer patients who took statins cholesterol lowering drugs showed improved overall and cancer-specific survival. “This study establishes a mechanistic link for these observations and highlights the potential of targeted fatty acid metabolism in remodeling the host’s antitumor immune response,” Lei said.
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