A team from Roswell Park Comprehensive Cancer Center has identified the beta-adrenergic receptor (β-AR) as a driver of immune suppression and cancer growth in response to chronic stress, opening the possibility of targeting this receptor in cancer therapy and prevention.
The study, titled “β-2-adrenergic receptor signaling regulates metabolic pathways critical to myeloid-derived suppressor cell function within the TME,” was published in Cell Reports.
Using a preclinical model of triple-negative breast cancer, a research team led by Hemn Mohammadpour, a postdoctoral research affiliate in the lab of Elizabeth Repasky, and Repasky, who is co-leader of the Cell Stress and Biophysical Therapies Program and the Dr. William Huebsch Professor in Immunology at Roswell Park, found that as tumors grow, they become more sensitive to stress signals coming from the nervous system.
Specifically, the researchers discovered that myeloid derived suppressor cells show an increase in the expression of β-AR. The findings will help researchers better understand why prolonged exposure to stress often makes the immune system less effective.
Several clinical trials are planned or underway to investigate which interventions are most effective at mitigating the effects of stress in patients with cancer. Roswell Park is currently studying the effects of combining the β-AR blocker propranolol, which is traditionally used to treat migraines and heart problems, with immunotherapy.
Co-authors include Philip McCarthy, professor of oncology and internal medicine and director of Roswell Park’s Transplant & Cellular Therapy Center; Scott Abrams, co-leader of Roswell Park’s Tumor Immunology and Immunotherapy Program; and Cameron MacDonald, a predoctoral trainee in immunology.
