Study Overview
A research team from the University of Michigan Rogel Cancer Center and School of Dentistry has identified a mechanism that may explain how obesity affects the ability of the immune system to respond to oral cancers.
The study, led by pathologist-immunologist Dr. Yu Leo Lei, is a significant step towards understanding the relationship between obesity and oral cancer.
The results of the study were published in Cell Reports. The team uncovered that obesity helps create a type of tumor microenvironment that promotes tumor progression.
The key to this lies in the interplay between saturated fatty acids, the STING-type-I interferon pathway, and a protein known as NLRC3.
Obesity and Oral Cancer: The Connection
While the links between obesity and various types of cancer, such as gastrointestinal tumors, breast cancer, pancreatic cancer, and ovarian cancer, are well known, the relationship between obesity and oral cancer has been underappreciated, according to Dr. Lei.
This new study sheds light on this connection.
The team’s research found that myeloid cells, a type of immune cell, in obese mice were less sensitive to STING agonists and were more suppressive of T cell activation compared to the myeloid cells from lean mice.
This feature led to the loss of immune subsets that were crucial for anti-tumor immunity within the tumor microenvironment.
Interestingly, the researchers discovered that saturated fatty acids can block the STING pathway, which is typically activated by DNA within cells and promotes the maturation of antigen-presenting cells, a crucial part of the immune response.
This blocking effect is mediated by the induction of the protein NLRC3.
Implications and Future Directions
Dr. Lei emphasized that this is the first study establishing a mechanistic link between obesity and immune escape in oral cancer, highlighting the potential translational implications of the research.
Obesity is a common comorbidity in cancer patients, and recent studies have shown that oral cancer patients on statins, medicines that lower cholesterol, demonstrated improved overall and cancer-specific survival.
This study suggests a mechanistic link for these clinical observations and underscores the potential of targeting fatty acids metabolism in changing the host anti-tumor immune response, according to Dr. Lei.
Looking ahead, the research team plans to explore how obesity regulates other immune-activating pathways and identify novel intervention targets for better oral cancer prevention in high-risk individuals.
However, more research needs to be done before these findings can be applied in the clinic.
This study highlights the importance of continuing to investigate the links between obesity and cancer, and how targeting metabolism might offer new strategies for cancer prevention and treatment.
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The study was published in Cell Reports.
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